Thursday, December 16, 2010

Markers for Medial Superior Olivary Neurons

This is an excellent reference for researchers looking for immunohistochemistry images of slice preparations of the Neurons in the medial superior olive (MSO). It also references use of our widely used and frequently published MAP2 (Microtubule associated protein 2).

Kiri Couchman, Benedikt Grothe and Felix Felmy. Medial Superior Olivary Neurons Receive Surprisingly Few Excitatory and Inhibitory Inputs with Balanced Strength and Short-Term Dynamics. The Journal of Neuroscience, December 15, 2010, 30(50):17111-17121; doi:10.1523/JNEUROSCI.1760-10.2010.

Summary: Neurons in the medial superior olive (MSO) process microsecond interaural time differences, the major cue for localizing low-frequency sounds, by comparing the relative arrival time of binaural, glutamatergic excitatory inputs. This coincidence detection mechanism is additionally shaped by highly specialized glycinergic inhibition. Traditionally, it is assumed that the binaural inputs are conveyed by many independent fibers, but such an anatomical arrangement may decrease temporal precision. Short-term depression on the other hand might enhance temporal fidelity during ongoing activity. For the first time we show that binaural coincidence detection in MSO neurons may require surprisingly few but strong inputs, challenging long-held assumptions about mammalian coincidence detection. This study exclusively uses adult gerbils for in vitro electrophysiology, single-cell electroporation and immunohistochemistry to characterize the size and short-term plasticity of inputs to the MSO. We find that the excitatory and inhibitory inputs to the MSO are well balanced both in strength and short-term dynamics, redefining this fastest of all mammalian coincidence detector circuits.

Related Reagents:
Neuronal-Glial Markers
-Astrocytes, Glia,
Microglia, Olidogodendrocytes, Progenitors and Schwann Cell Markers
Stem Cell Research Antibodies

Stem Cell Research Reagents

Primary Neurons and Astrocytes
human, rat and mouse neurons and astrocytes.

Saturday, November 27, 2010

Fragile-X, Astrocytes and BMC Image of the Month

Dr. Laurie Doering and his team at McMaster University are discovering root causes of Fragile X Syndrome. A disease manifested by cognitive impairment, attention deficit and autistic behaviours.

I wanted to share highlights and links to a recent publication as it contains interesting conclusions and some of the best multiple label staining of combined embryonic rat and mouse neurons-astrocytes cultures I have seen. No wonder that this is a highly accessed Biomed Central Article and includes the image of the month. The featured  image references use of our MAP-2 antibody.

Shelley Jacobs , Meera Nathwani and Laurie C Doering. Fragile X astrocytes induce developmental delays in dendrite maturation and synaptic protein expression. BMC Neuroscience 2010, 11:132doi:10.1186/1471-2202-11-132.

Conclusions: These experiments are the first to establish a role for astrocytes in the delayed growth characteristics and abnormal morphological features in dendrites and synapses that characterize the Fragile X syndrome.

Image: Co-culture of embryonic mouse hippocampal neurons and astrocytes. Primary embryonic hippocampal neurons at 7 days in vitro, were stained with Microtubule Associated Protein-2 (MAP, green) to enable the visualization of the dendritic arbors. These neurons were cultured on top of a monolayer of primary cortical astrocytes, stained with an antibody directed against Glial Fibrillary Acidic Protein (GFAP, red). The cell nuclei were visualized by staining with 4',6-diamidino-2-phenylindole (DAPI, blue).

Related Links:
Neuronal-Glial Markers-Astrocytes, Glia, Microglia, Olidogodendrocytes, Progenitors and Schwann Cell Markers
Neurofilament or NF Antibodies
Stem Cell Research Antibodies
Stem Cell Research Reagents
Primary Neurons and Astrocytes-Primary human, rat and mouse neurons and astrocytes.

Thursday, November 18, 2010

Cancer-Induced Bone Pain

Bone crushing pain. This describes pain of the highest order. Our friend, Dr. Joseph Ghilardi, VAMC-Mpls. and his colleague, Dr. Patrick Manthy are finding the root causes of the intense and growing pain suffered by Cancer Victims. Here are highlights of a recent study:

Pain frequently accompanies cancer. What remains unclear is why this pain frequently becomes more severe and difficult to control with disease progression. Here we test the hypothesis that with disease progression, sensory nerve fibers that innervate the tumor-bearing tissue undergo a pathological sprouting and reorganization, which in other nonmalignant pathologies has been shown to generate and maintain chronic pain. Injection of canine prostate cancer cells into mouse bone induces a remarkable sprouting of calcitonin gene-related peptide (CGRP+) and neurofilament 200 kDa (NF200+) sensory nerve fibers. Nearly all sensory nerve fibers that undergo sprouting also coexpress tropomyosin receptor kinase A (TrkA+). This ectopic sprouting occurs in sensory nerve fibers that are in close proximity to colonies of prostate cancer cells, tumor-associated stromal cells and newly formed woven bone, which together form sclerotic lesions that closely mirror the osteoblastic bone lesions induced by metastatic prostate tumors in humans. Preventive treatment with an antibody that sequesters nerve growth factor (NGF), administered when the pain and bone remodeling were first observed, blocks this ectopic sprouting and attenuates cancer pain. Interestingly, reverse transcription PCR analysis indicated that the prostate cancer cells themselves do not express detectable levels of mRNA coding for NGF. This suggests that the tumor-associated stromal cells express and release NGF, which drives the pathological reorganization of nearby TrkA+ sensory nerve fibers. Therapies that prevent this reorganization of sensory nerve fibers may provide insight into the evolving mechanisms that drive cancer pain and lead to more effective control of this chronic pain state.

Image: Image:Shows rat mixed neuron/glial cultures stained with mouse monoclonal antibody to neurofilament subunit NF-L clone 7D1 (green) and chicken antibody to neurofilament NF-H. This antibody binds primarily to the phosphorylated axonal forms of NF-H, in contrast to the NF-L antibody which stains both axonal and dendritic/perikaryal neurofilaments. The NF-L antibody therefore reveals a prominent cell body in green, while the surrounding axonal profiles are orange, since the are bound by both NF-L and the chicken NF-H antibody. Blue is a DNA stain. Protocol on data sheet.

 Juan M. Jimenez-Andrade, Aaron P. Bloom, James I. Stake, William G. Mantyh, Reid N. Taylor, Katie T. Freeman, Joseph R. Ghilardi, Michael A. Kuskowski, and Patrick W. Mantyh Pathological Sprouting of Adult Nociceptors in Chronic Prostate Cancer-Induced Bone Pain. J. Neurosci., Nov 2010; 30: 14649 - 14656 ; doi:10.1523/JNEUROSCI.3300-10.2010
Here're several other pubs referencing use of our antibodies in studying bone cancer pain:

Kyle G. Halvorson, BA, Molly A. Sevcik, BA, Joseph R. Ghilardi, BS, BA, Lucy J. Sullivan, BA, Nathan J. Koewler, BS, Frieder Bauss, PhD, and Patrick W. Mantyh, PhD. Intravenous Ibandronate Rapidly Reduces Pain, Neurochemical Indices of Central Sensitization, Tumor Burden, and Skeletal Destruction in a Mouse Model of Bone Cancer. Published online 2008 April 14. doi: 10.1016/j.jpainsymman.2007.10.005 (DYN, polyclonal guinea pig anti-rat, 1:1,000; Neuromics, Minneapolis, MN)...

Timothy K. Y. Kaan, Ping K. Yip, Sital Patel, Meirion Davies, Fabien Marchand, Debra A. Cockayne, Philip A. Nunn, Anthony H. Dickenson, Anthony P. D. W. Ford, Yu Zhong, Marzia Malcangio, and Stephen B. McMahon Systemic blockade of P2X3 and P2X2/3 receptors attenuates bone cancer pain behaviour in rats. Brain, September 2010; 133: 2549 - 2564.
......Slides were then incubated with rabbit anti-P2X3 (1:2000, Neuromics) and sheep anti-calcitonin gene-related peptide (1:1000, Biomol...anti-beta-III-tubulin (1:4000, Promega) and guinea pig anti-P2X3 (1:100, Neuromics). The next day, after three washes with phosphate-buffered......

I will keep you posted on this important topic.

Wednesday, November 10, 2010

Our TRPV1 Antibodies Rock

We now have 40 publications referencing use of our TRP Antibodies in multiple applications. Here are the October-November 2010 publications referencing use of these antibodies:

VR1 N-Terminus (TRPV1)-Rabbit

T. Wu, L. Song, X. Shi, Z. Jiang, J. Santos-Sacchi and A.L. Nuttal. Effect of capsaicin on potassium conductance and electromotility of guinea pig outer hair cell. doi:10.1016/j.heares.2010.10.010
...anti-TRPV1 (rabbit polyclonal, RA10110, Neuromics, Edina, MN, USA) diluted to 1:500 with 1% BSA-PBS...antibody (TRPV-1) and its blocking peptide (104 M) (Neuromics, Edina, MN, USA)...

(TRPV1) - mouse specific
Julie A. Christianson, Klaus Bielefeldt, Sacha A. Malin and Brian M. Davis. Neonatal colon insult alters growth factor expression and TRPA1 responses in adult mice. Pain Volume 151, Issue 2, November 2010, Pages 540-549.
...primary antiserum to TRPV1 (1:4000; Neuromics, Minneapolis, MN; cat# RA14113)...

VR1 C-terminus (TRPV1)-Guinea Pig
N. Schuelert, C. Zhang, A.J. Mogg, L.M. Broad, D.L. Hepburn, E.S. Nisenbaum, M.P. Johnson and J.J. McDougal. Paradoxical effects of the cannabinoid CB2 receptor agonist GW405833 on rat osteoarthritic knee joint pain. Osteoarthritis and Cartilage Volume 18, Issue 11, November 2010, Pages 1536-1543.
...primary antiserum to TRPV1 (1:4000; Neuromics, Minneapolis, MN; cat# RA14113)...

Mariusz Mucha, Lezanne Ooi, John E. Linley, Pawel Mordaka, Carine Dalle, Brian Robertson, Nikita Gamper, and Ian C. Wood Transcriptional Control of KCNQ Channel Genes and the Regulation of Neuronal Excitability.
J. Neurosci., Oct 2010; 30: 13235 - 13245 ; doi:10.1523/JNEUROSCI.1981-10.2010
...1:1000 guinea pig anti-TRPV1 (Neuromics)...

Related Reagents:
All TRP Antibodies
Pain and Inflammation Research Antibodies
Neurotransmission -Neurotransmission Research Antibody Categories

Thursday, October 28, 2010

Vitamin A Deficiency and Hirschsprung Disease

Dr. Robert Heuckeroth and his team and Washington University recently published more results on the link between maternal Vitamin A Deficiency and Hirschsprung Disease. It underscores the importance of maternal vitamin A nutrition for preventing the diease penetrance and expressitivity:
Ming Fu, Yoshiharu Sato, Ariel Lyons-Warren, Bin Zhang, Maureen A. Kane, Joseph L. Napoli and Robert O. Heuckeroth. Vitamin A facilitates enteric nervous system precursor migration by reducing Pten accumulation. Development 137, 631-640 (2010) doi:10.1242/dev.040550.
Hirschsprung disease is a serious disorder of enteric nervous system (ENS) development caused by the failure of ENS precursor migration into the distal bowel. We now demonstrate that retinoic acid (RA) is crucial for GDNF-induced ENS precursor migration, cell polarization and lamellipodia formation, and that vitamin A depletion causes distal bowel aganglionosis in serum retinolbinding-protein-deficient (Rbp4–/–) mice. Ret heterozygosity increases the incidence and severity of distal bowel aganglionosis induced by vitamin A deficiency in Rbp4–/– animals. Furthermore, RA reduces phosphatase and tensin homolog (Pten) accumulation in migrating cells, whereas Pten overexpression slows ENS precursor migration. Collectively, these data support the hypothesis that vitamin A deficiency is a non-genetic risk factor that increases Hirschsprung disease penetrance and expressivity, suggesting that some cases of Hirschsprung disease might be preventable by optimizing maternal nutrition.

By the way, the lab has been an ongoing consumer of our Ret Antibody and referenced use of this antibody in the publication.

Image: E12.5 mouse mid-gut slices were cultured to allow crest-derived cells to migrate onto the dish in response to GDNF. Cultures were maintained for 16 hours without added retinoic acid.

Related Reagents:

Ret (C-Terminus Fused)

Ret-Fluorescein Labeled

Ret-Allophycocyanin Labeled

Ret-Phycoerythrin Labeled

Neurotrophins and Growth Factor Antibodies

Neurotrophins-Neuron/Glial Marker
Recombinant Proteins

Neuron/Glial Markers

Stem Cell Research Reagents

Thursday, October 21, 2010

Stems Cells and SCI

This is fascinating and encouraging to sufferers of Spinal Cord Injury:

ScienceDaily (Oct. 9, 2010) — Researchers at Karolinska Institutet have shown how stem cells, together with other cells, repair damaged tissue in the mouse spinal cord. The results are of potential significance to the development of therapies for spinal cord injury:

Saturday, October 09, 2010

Enhancing Neurite Outgrowth

We are pleased to announce the addition of new proteins to our Axon Growth and Guidance category. These are designed to enhance neurite out growth.

Catalog #TypeSpeciesSizePrice
NGF-b, NSO Derived
ProteinH; M; R100 ug$285
NGF-b, NSO Derived, CFPR15084CFProteinH; M; R100 ug$285
S100A13, CFPR15085CF-50ProteinH; R50 ug$315
Slit1PR15075-50ProteinCh; H50 ug$315
Slit2, CHO
ProteinCh; H50 ug$315

Image: Cultured chick dorsal root ganglion neurons were grown in the presence of recombinant human NGF-b with (A) or without (B) recombinant mouse Slit2. The presence of the Slit2 protein signifi cantly enhanced neurite outgrowth.

Wednesday, September 22, 2010

Glutaredoxin 2 prevents aggregation of mutant SOD1

Our PTEN-induced kinase, PINK1 or PARK6 Antibody is an excellent marker for Amyotrophic Lateral Sclerosis (ALS) and Parkinson's Disease (PD) researchers.

Here's  new publication referencing use of this antibody:  Alberto Ferri, Paolo Fiorenzo, Monica Nencini, Mauro Cozzolino, Maria Grazia Pesaresi, Cristiana Valle, Sara Sepe, Sandra Moreno, and Maria Teresa Carrì. Glutaredoxin 2 prevents aggregation of mutant SOD1 in mitochondria and abolishes its toxicity.
Hum. Mol. Genet., first published on Sep 20, 2010 as doi: doi:10.1093/hmg/ddq383

Vulnerability of motoneurons in amyotrophic lateral sclerosis (ALS) arises from a combination of several mechanisms, including protein misfolding and aggregation, mitochondrial dysfunction and oxidative damage. Protein aggregates are found in motoneurons in models for ALS linked to a mutation in the gene coding for Cu,Zn superoxide dismutase (SOD1) and in ALS patients as well. Aggregation of mutant SOD1 in the cytoplasm and/or into mitochondria has been repeatedly proposed as a main culprit for the degeneration of motoneurons. It is, however, still debated whether SOD1 aggregates represent a cause, a correlate or a consequence of processes leading to cell death. We have exploited the ability of glutaredoxins (Grxs) to reduce mixed disulfides to protein thiols either in the cytoplasm and in the IMS (Grx1) or in the mitochondrial matrix (Grx2) as a tool for restoring a correct redox environment and preventing the aggregation of mutant SOD1. Here we show that the overexpression of Grx1 increases the solubility of mutant SOD1 in the cytosol but does not inhibit mitochondrial damage and apoptosis induced by mutant SOD1 in neuronal cells (SH-SY5Y) or in immortalized motoneurons (NSC-34). Conversely, the overexpression of Grx2 increases the solubility of mutant SOD1 in mitochondria, interferes with mitochondrial fragmentation by modifying the expression pattern of proteins involved in mitochondrial dynamics, preserves mitochondrial function and strongly protects neuronal cells from apoptosis. The toxicity of mutant SOD1, therefore, mostly arises from mitochondrial dysfunction and rescue of mitochondrial damage may represent a promising therapeutic strategy.
Related Reagents:
PARK2 Co-regulated (PACRG)
PARK7 (DJ-1)
LRRK2 (PARK8)                        
Neurodegenerative Disease Research Antibodies                          

Neurodegenerative Disease Research Proteins
Neurotransmission -Neurotransmission Research Antibody Categories                         
Neurotrophins and Growth Factor Antibodies
Neuron-Glial Expressed-Includes Neurotrophin Proteins
Apoptosis Research Reagents-Apoptosis Categories-includes: detection kits, antibodies and proteins

Primary Neurons and Astrocytes -Primary human, rat and mouse neurons and astrocytes by Category

Wednesday, September 15, 2010

TRHR1 and LepRb receptors and Thermogenesis

I would like to thank Montina Van Meter, Lab Manager, Autonomic Neuroscience at Pennington Biomedical Research Center, for alerting me to this just published study. Included are excellent images of stained LepRb (OB-Rb) and GAD1 expressing neurons localized in loose clusters of cells in the DMN, NST, and the VLM.

This study focus on identifying loci in the hindbrain where leptin and TRH act synergistically to increase thermogenesis. Since thermogenic processes are at the root of how our bodies regulate energy, understanding the related expression and signaling pathways could be key to finding therapies for obesity.

Maria J. Barnes, Richard C. Rogers, Montina J. Van Meter and Gerlinda E. Hermann. Co-localization of TRHR1 and LepRb receptors on neurons in the hindbrain of the rat. doi:10.1016/j.brainres.2010.07.094

Example images: Distribution of LepRb+ fibers in hindbrain. LepRb-ir (red) fibers and varicosities are seen among TRHR1-ir (green) cells and fibers. These red and green fibers are adjacent and co-mingle but do not show co-localization of receptors. This pattern is seen in (A) fascicles of the solitary tract (ST); (B) raphe pallidus (RP), and (C) raphe obscurrus (RO). (D) Border between the medial solitary nucleus (NST) and the area postrema (AP; white dashed line) showing an abundance of LepRb-ir (red) fibers and
 neurons (white arrows for selected neurons) in the NST but not the AP. (E) LepRb-ir staining is suppressed by pretreatment of tissue with LepRb epitope blocking peptide. (F) TRHR1-ir staining is suppressed by treatment with excess TRHR1. Scale bar A–D=100 microns; E, F=300 microns. cc=central canal.
Abstract: We have reported a highly cooperative interaction between leptin and thyrotropin releasing hormone (TRH) in the hindbrain to generate thermogenic responses (Hermann et al., 2006) (Rogers et al., 2009). Identifying the locus in the hindbrain where leptin and TRH act synergistically to increase thermogenesis will be necessary before we can determine the mechanism(s) by which this interaction occurs. Here, we performed heat-induced epitope recovery techniques and in situ hybridization to determine if neurons or afferent fibers in the hindbrain possess both TRH type 1 receptor and long-form leptin receptor [TRHR1; LepRb, respectively]. LepRb receptors were highly expressed in the solitary nucleus [NST], dorsal motor nucleus of the vagus [DMN] and catecholaminergic neurons of the ventrolateral medulla [VLM]. All neurons that contained LepRb also contained TRHR1. Fibers in the NST and the raphe pallidus [RP] and obscurrus [RO] that possess LepRb receptors were phenotypically identified as glutamatergic type 2 fibers (vglut2). Fibers in the NST and RP that possess TRHR1 receptors were phenotypically identified as serotonergic [i.e., immunopositive for the serotonin transporter; SERT]. Co-localization of LepRb and TRHR1 was not observed on individual fibers in the hindbrain but these two fiber types co-mingle in these nuclei. These anatomical arrangements may provide a basis for the synergy between leptin and TRH to increase thermogenesis.

Related Reagents:
Leptin and Leptin Receptor Antibodies
Leptin Proteins

Tuesday, September 14, 2010

Isolation of Medulloblastoma Stem Cells (Video Protocol)

I am pleased to present this excellent video. It also has excellent images using key stem cell markers as the cells undergo differentiation:

Sep 1, 2010 ... GFAP antibody, Neuromics, CH22102,
Chicken, 1:1000. Tuj1 antibody, Sigma, T5076, Mouse, 1:2000. NeuN
antibody, Millipore, MAB377, Mouse, ...

Thursday, September 09, 2010

Potential Therapeutic Targets for Bone Cancer Pain-P2X Receptors

Cancer pain is difficult to treat as it appears to be driven simultaneously by inflammatory, neuropathic and tumorigenic mechanisms. I have reported on multiple occasions publication referencing use of our Pain and Inflammation Research Antibodies in studying bone cancer pain.

I would like to alert you to the latest reference:

Timothy K. Y. Kaan, Ping K. Yip, Sital Patel, Meirion Davies, Fabien Marchand, Debra A. Cockayne, Philip A. Nunn, Anthony H. Dickenson, Anthony P. D. W. Ford, Yu Zhong, Marzia Malcangio, and Stephen B. McMahon Systemic blockade of P2X3 and P2X2/3 receptors attenuates bone cancer pain behaviour in rats. Brain, September 2010; 133: 2549 - 2564.

......Slides were then incubated with rabbit anti-P2X3 (1:2000, Neuromics) and sheep anti-calcitonin gene-related peptide (1:1000, Biomol...anti-beta-III-tubulin (1:4000, Promega) and guinea pig anti-P2X3 (1:100, Neuromics). The next day, after three washes with phosphate-buffered......

Summary: Pain remains an area of considerable unmet clinical need, and this is particularly true of pain associated with bone metastases, in part because existing analgesic drugs show only limited efficacy in many patients and in part because of the adverse side effects associated with these agents. An important issue is that the nature and roles of the algogens produced in bone that drive pain-signalling systems remain unknown. Here, we tested the hypothesis that adenosine triphosphate is one such key mediator through actions on P2X3 and P2X2/3 receptors, which are expressed selectively on primary afferent nocioceptors, including those innervating the bone. Using a well-established rat model of bone cancer pain, AF-353, a recently described potent and selective P2X3 and P2X2/3 receptor antagonist, was administered orally to rats and found to produce highly significant prevention and reversal of bone cancer pain behaviour. This attenuation occurred without apparent modification of the disease, since bone destruction induced by rat MRMT-1 carcinoma cells was not significantly altered by AF-353. Using in vivo electrophysiology, evidence for a central site of action was provided by dose-dependent reductions in electrical, mechanical and thermal stimuli-evoked dorsal horn neuronal hyperexcitability following direct AF-353 administration onto the spinal cord of bone cancer animals. A peripheral site of action was also suggested by studies on the extracellular release of adenosine triphosphate from MRMT-1 carcinoma cells. Moreover, elevated phosphorylated-extracellular signal-regulated kinase expression in dorsal root ganglion neurons, induced by co-cultured MRMT-1 carcinoma cells, was significantly reduced in the presence of AF-353. These data suggest that blockade of P2X3 and P2X2/3 receptors on both the peripheral and central terminals of nocioceptors contributes to analgesic efficacy in a model of bone cancer pain. Thus, systemic P2X3 and P2X2/3 receptor antagonists with central nervous system penetration may offer a promising therapeutic tool in treating bone cancer pain.

Related Reagents:

All Purinergic Receptors
Neurotransmission Research Antibodies

Sunday, August 08, 2010

Angiogenesis Research Reagents

The processes of angiogenesis and neurogenesis show striking similarities. Given our strong roots in providing Neuroscience research reagents, it is a natural extension for us to provide potent reagents for the studying the growth of new blood vessels.

Angiogensis processes are important for healing wounds and for restoring blood flow to tissues after injury or insult. In females, it also occurs during the monthly reproductive cycle and during pregnancy(to build the placental circulation between mother and fetus.

Images: Increased arteriogenesis and hyperemia in TSP2-null mice. Smooth muscle actin-positive and ephrin B2-positive vessels in WT (F, H) and TSP2-null (G, I). DOI: 10.2353/ajpath.2008.080128.

Angiogenesis-dependent diseases result when new blood vessels either grow excessively or insufficiently. These disease include: cancers, diabetic blindness, age-related macular degeneration, rheumatoid arthritis, psoriasis, neurodegeneration and many more.

Product Categories

Thursday, July 29, 2010

Let-7 microRNAs and Nociceptive Pain

Our Opioid Receptor Antibodies have set a potent standard for studying Nociceptive and Neuropathic Pain. Related Publications.

We want to recognize Dr. Zaijie Jim Wang and his team for being the first to use our Mu Opioid Receptor for studying the potential role of microRNAs in Nociception.

Ying He, Cheng Yang, Chelsea M. Kirkmire, and Zaijie Jim Wang. Regulation of Opioid Tolerance by let-7 Family MicroRNA Targeting the µ Opioid Receptor. The Journal of Neuroscience, July 28, 2010, 30(30):10251-10258; doi:10.1523/JNEUROSCI.2419-10.2010
Abstract: MicroRNA has emerged as a critical regulator of neuronal functions. This study aimed to test whether let-7 microRNAs can regulate the µ opioid receptor (MOR) and opioid tolerance. Employing bioinformatics, we identified a let-7 binding site in the 3'-untranslated region (UTR) of MOR mRNA, which was experimentally confirmed as a direct target of let-7. The repressive regulation of MOR by let-7 was revealed using a LNA-let-7 inhibitor to knockdown let-7 in SH-SY5Y cells. Conversely, morphine significantly upregulated let-7 expression in SH-SY5Y cells and in a mouse model of opioid tolerance. The LNA-let-7 inhibitor decreased brain let-7 levels and partially attenuated opioid antinociceptive tolerance in mice. Although chronic morphine treatment did not change overall MOR transcript, polysome-associated mRNA declined in a let-7-dependent manner. let-7 was identified as a mediator translocating and sequestering MOR mRNA to P-bodies, leading to translation repression. These results suggest that let-7 plays an integral role in opioid tolerance.

  • Western blot analysis. Western blot analysis was performed as previously described (Tang et al., 2006) using the anti-µ opioid receptor antibody (1:1000; Neuromics). The expression of β-actin was similarly determined from the same blots using a monoclonal antibody (1:10,000; Sigma).
  • For immunofluorescence analysis, the antibody for hDcp1a (Santa Cruz Biotechnology) and MOR were used at 1:500 and 1:5000 dilutions, respectively. Secondary anti-goat and anti-mouse antibodies labeled with Alexa 488 and Alexa 594 fluorochromes (Invitrogen), respectively, were used at 1:500 dilutions.

Related Reagent Links:
All Opioid Receptor Antibodies

Pain and Inflammation
Neurotransmission Research Antibodies
-GPCRs, Ligand Gated Ion Channels,
Biogenic Amines and more
i-Fect Transfection Kit
-gene silencing of DOR,
NaV1.8 tetrodotoxin-resistant sodium channel, NTS2 and more in-vitro and in vivo
Primary Neurons and Astrocytes
-Primary human,
rat and mouse neurons and astrocytes 

Monday, July 26, 2010

δ- and μ-opioid receptors co-expression and Nociceptive Pain

Dr. Tomas Hokfelt and his team at Karolinska Institute recently published use of our Opioid Receptor Antibodies and Substance P Antibody.They show the interplay of DOR and MOR in modulation of nociceptive afferent transmission and opioid analgesia.

Hai-Bo Wanga, Bo Zhaoa, Yan-Qing Zhonga, Kai-Cheng Li, Zi-Yan Li, Qiong Wang, Yin-Jing Lua, Zhen-Ning Zhang, Shao-Qiu He, Han-Cheng Zheng, Sheng-Xi Wu, Tomas G. M. Hökfelt, Lan Baob, and Xu Zhanga. Coexpression of δ- and μ-opioid receptors in nociceptive sensory neurons. PNAS July 20, 2010 vol. 107 no. 29 13117-13122.

Immunostaining. Adult rats, mice, and Oprd1 exon 1-deleted mice were fixed. Cryostat sections of L4 and L5 DRGs and spinal cord segments were processed for immunofluorescence staining (13) with Rb anti-DOR13–17 (1:2,000–1:60,000; DiaSorin and 1:4,000–1:60,000; Neuromics), Rb anti-DOR12–18 (1:30,000–1:120,000; Alomone), Rb anti-DOR1358–372 (1:1,000–1:2,000; Lifespan Biosciences), Rb anti-MOR (1:1,000; Neuromics); guinea pig anti-SP (1:500; Neuromics), and mouse anti-CGRP (1:1,000; Biogenesis) antibodies. IB4-labeling was carried out with fluorescein-labeled GSL I-IB4 (1:200). The Myc-DOR1–transfected HEK293 cells and neurons were fixed and processed with mouse anti-Myc antibodies (1:500; DSHB). Nuclear DAPI staining was used to indicate HEK293 cells in control experiments.

Images: Distinct distribution patterns of DORs in subsets of DRG neurons of mice. Immunostaining with antibodies against DOR13–17 [A: 1:30,000, antibody 1 (ab #1); DiaSorin and C: antibody 2 (ab #2); Neuromics] shows DORs in small DRG neurons and afferent fibers in spinal laminae I–II. This immunostaining pattern is abolished by the antiserum preabsorption or the deletion of Oprd1 exon 1. Reduction in immunostaining is quantitatively assayed by determining the percentage of positive DRG neurons (B; n = 6) and fluorescence intensity (Ifluo.) in the laminae I–II (D; n = 5). **P < 0.01; ***P < 0.001. (Scale bars: A and C, 40 μm.). DOR labeling (anti-DOR13–17, 1:30,000; DiaSorin) associated with vesicles in peptidergic small DRG neurons (E and F) is absent in Oprd1 exon 1-deleted mice (G). Colocalization of DORs and neuropeptides is shown by correlated peaks of Ifluo. measured along lines. (Scale bar: 8 μm.) (H) Immunostaining with antibodies against DOR12–18 (1:60,000; Alomone) shows the presence of DORs on the cell surface of large DRG neurons of mice. (Scale bar: 25 μm.) This staining pattern is abolished by preabsorption and is absent in Oprd1 exon 1-deleted mice. (Scale bar: 80 μm.) (I) Triple-immunostaining shows that DOR+ large DRG neurons contain neither SP nor CGRP. (Scale bar: 80 μm.)

Immunoblotting.The samples were processed for SDS/PAGE, transferred, probed with Rb antibodies against MOR (1:500; Neuromics), phospho-DOR1 (1:1,000; Neuromics), phospho-MOR (1:1,000; Neuromics), Myc (1:500; DSHB), Flag (1:1,000; Sigma), or actin (1:50,000; Chemicon) and visualized with enhanced chemiluminescence (19).

Featured and Related Reagents:

Mu Opioid Receptor-Rabbit

Mu Opioid Receptor-Guinea Pig

Delta Opioid Receptor 3-17

Delta Opioid Receptor 358-372

Delta Opioid Receptor 358-372

Kappa Opioid Receptor

phospho-Mu Opioid Receptor (Ser375)


ORL 1-Pure

ORL1-Whole Serum

All Opioid Receptor Antibodies

Pain and Inflammation

Neurotransmission Research Antibodies
-GPCRs, Ligand Gated Ion
Channels, Biogenic Amines and more

i-Fect Transfection Kit
-gene silencing
of DOR, NaV1.8 tetrodotoxin-resistant sodium channel, NTS2 and more
in-vitro and in vivo

Primary Neurons and Astrocytes
human, rat and mouse neurons and astrocytes

Monday, July 19, 2010

Staining Neuron-Glial Cultures-Related Markers

I have been receiving a growing number of requests for best techniques related to staining cultures of primary neurons and glia. I wanted to share this short, step by step protocol.

These requests are often catalyzed by a search of our growing Neuron/Glial Markers catalog. The objective being to find the right markers for a particular assay. I wanted to share examples of the potency of several Neurofilament or NF markers for labeling neurons:

1. Neurofilament NF-L-Mouse Monoclonal Antibody (Clone: DA2) and Neurofilament alpha-internexin/NF66-Whole Serum-Rabbit Antibody

Images: Cells grown from adult rat brainLarge cell in middle is stained with mouse monoclonal to NF-L clone DA2 (green). Another type of neuronal lineage cell was stained with rabbit polyclonal to alpha-internexin (red). These cells were mitotic but had several characteristics of neurons. Rat spinal cord homogenate showing the major intermediate filament proteins of the nervous system (lane 1). The remaining lanes show blots of this material stainted with various antibodies including NF-L. Protocols on data-sheet.

2. Neurofilament NF-H, phosphylated-Mouse Monoclonal and Neurofilament NF-L-Purified Chicken Polyclonal.

Image: View of mixed neuron/glial cultures stained with chicken polyclonal NF-L (red) and phosphorylated NF-H The NF-L protein is assembled into neurofilaments which are found throughout the axons, dendrites and perikarya of these cells. In contrast the phosphorylated NF-H has a much rmore restricted expression pattern, being found only in developed axonal neurofilaments. Since both proteins are found in neurofilaments, the red and green patterns overlap, so that neurofilaments containing NF-L and phosphorylated NF-H appear yellowish. In contrast neurofilaments containing only NF-L appear red. Protocol on datasheet.

Neurofilament Markers

Tuesday, July 06, 2010

TRPV1 & P2X3-Daily Double

Low pH and Chronic Muscle Pain

Our Pain and Inflammation Antibodies are routinely used for chronic pain. I would like to highlight a recent publication referencing use of our  Guinea Pig TRPV1 and Pig 2X3 Antibodies and Blocking Peptides:

Low pH leads to changes in several electrical properties of MSA, including initiation of ectopic action potentials which could propagate centrally but could also invade the peripheral endings causing glutamate release and activation of nearby nociceptors within the spindle capsule. This peripheral drive could contribute both to the transition to, and maintenance of, persistent muscle pain as seen in some “functional” pain syndromes.

Images: Photomicrographs of trigeminal ganglion neurons stained with TRPV1 and P2X3.
Related Reagents:

Primary Neurons and Astrocytes-Primary human, rat and mouse neurons and astrocytes

Monday, June 28, 2010

Otx2 (Orthodenticle Homeobox 2) and Parkinson's Disease

Our Otx2 Antibody is a potent marker for Human, Mouse and Rat Midbrain Dopamanergic Progenitors.

This is confirmed by a recent publication by Dr. Ole Isaacson et al:

Chee Yeun Chung, Pawel Licznerski, Kambiz N. Alavian, Antonio Simeone, Zhicheng Lin, Eden Martin, Jeffery Vance and Ole Isacson. The transcription factor orthodenticle homeobox 2 influences axonal projections and vulnerability of midbrain dopaminergic neurons. Brain Advance Access published online on June 23, 2010 Brain, doi:10.1093/brain/awq142... anti-Otx2 (Neuromics, 1:500)...

Abstract: Two adjacent groups of midbrain dopaminergic neurons, A9 (substantia nigra pars compacta) and A10 (ventral tegmental area), have distinct projections and exhibit differential vulnerability in Parkinson’s disease. Little is known about transcription factors that influence midbrain dopaminergic subgroup phenotypes or their potential role in disease. Here, we demonstrate elevated expression of the transcription factor orthodenticle homeobox 2 in A10 dopaminergic neurons of embryonic and adult mouse, primate and human midbrain. Overexpression of orthodenticle homeobox 2 using lentivirus increased levels of known A10 elevated genes, including neuropilin 1, neuropilin 2, slit2 and adenylyl cyclase-activating peptide in both MN9D cells and ventral mesencephalic cultures, whereas knockdown of endogenous orthodenticle homeobox 2 levels via short hairpin RNA reduced expression of these genes in ventral mesencephalic cultures. Lack of orthodenticle homeobox 2 in the ventral mesencephalon of orthodenticle homeobox 2 conditional knockout mice caused a reduction of midbrain dopaminergic neurons and selective loss of A10 dopaminergic projections. Orthodenticle homeobox 2 overexpression protected dopaminergic neurons in ventral mesencephalic cultures from Parkinson’s disease-relevant toxin, 1-methyl-4-phenylpyridinium, whereas downregulation of orthodenticle homeobox 2 using short hairpin RNA increased their susceptibility. These results show that orthodenticle homeobox 2 is important for establishing subgroup phenotypes of post-mitotic midbrain dopaminergic neurons and may alter neuronal vulnerability.

Image: Characterization of the human neuroectodermal precursors. Otx2 Staining of forebrain-midbrain rosettes (dilution 1:1000).

Related Reagents to Consider:

Friday, June 25, 2010

Nestin as a Marker for Astrocytomas

I recently highlighted the growing parade of pubs referencing use of our reagents for Cancer Research.

I would like to add a new one. Angogenesis of Astrocytomas show stem like properties. This makes our Nestin Antibodies excellent markers.

J H Tchaicha, A K Mobley, M G Hossain, K D Aldape and J H McCarty. A mosaic mouse model of astrocytoma identifies αvβ8 integrin as a negative regulator of tumor angiogenesis. Oncogene , (7 June 2010) doi:10.1038/onc.2010.199...chicken anti-Nestin IgY (Neuromics, Edina, MN, USA)...

Abstract: Angiogenesis involves a complex set of cell–cell and cell–extracellular matrix (ECM) interactions that coordinately promote and inhibit blood vessel growth and sprouting. Although many factors that promote angiogenesis have been characterized, the identities and mechanisms of action of endogenous inhibitors of angiogenesis remain unclear. Furthermore, little is known about how cancer cells selectively circumvent the actions of these inhibitors to promote pathological angiogenesis, a requisite event for tumor progression. Using mosaic mouse models of the malignant brain cancer, astrocytoma, we report that tumor cells induce pathological angiogenesis by suppressing expression of the ECM protein receptor αvβ8 integrin. Diminished integrin expression in astrocytoma cells leads to reduced activation of latent TGFβs, resulting in impaired TGFβ receptor signaling in tumor-associated endothelial cells. These data reveal that astrocytoma cells manipulate their angiogenic balance by selectively suppressing αvβ8 integrin expression and function. Finally, these results show that an adhesion and signaling axis normally involved in developmental brain angiogenesis is pathologically exploited in adult brain tumors.

Related Reagents:

Nestin Mouse Monoclonal-Cat#:MO15012

Nestin-Mouse Monoclonal-Cat#:MO15056

Nestin-Goat Polyclonal

Stem Cell Research Reagents

Friday, June 11, 2010

Cancer Reagents Pubs-Capabilities Update

We continue to grow our capaibilities and abilities to serve Cancer Researchers.

We recently highlighted the potency of our i-Fect ™ siRNA transfection kits for deliveriny siRNA to glioblastomas.

Joseph George, Naren L. Banik, Swapan K. Ray. Combination of hTERT Knockdown and IFN-γ Treatment Inhibited Angiogenesis and Tumor Progression in Glioblastoma. Clin Cancer Res 2009;15(23):7186–95

...with i-Fect transfection reagent (Neuromics) to obtain 5 μg DNA/10 μL of injection volume...

Here're several new publications highlighting use of our Cancer Research Antibodies:

Mauricio P. Pinto, Melanie M. Badtke, Michelle L. Dudevoir, J. Chuck Harrell, Britta M. Jacobsen and Kathryn B. Horwitz. Vascular Endothelial Growth Factor Secreted by Activated Stroma Enhances Angiogenesis and Hormone-Independent Growth of Estrogen Receptor–Positive Breast Cancer. Cancer Research 70, 2655, April 1, 2010. Published Online First March 23, 2010; doi: 10.1158/0008-5472.CAN-09-4373 © 2010 American Association for Cancer Research.

...Phosphorylated extracellular signal-regulated kinase (p-ERK) was assayed by immunohistochemistry (rabbit polyclonal; Neuromics). Statistical analyses Data were analyzed with GraphPad software using either Student's t test or ANOVA followed by a Tukey's...

Nina Bergelin, Christoffer Löf, Sonja Balthasar, Veronica Kalhori, and Kid Törnquist. S1P1, and VEGFR-2 Form a Signaling Complex with Extracellularly Regulated Kinase 1/2 and Protein Kinase C-alpha Regulating ML-1 Thyroid Carcinoma Cell Migration. This version published online on May 25, 2010. Endocrinology, doi:10.1210/en.2009-1387

...conjugated goat antirabbit from Bio-Rad Laboratories (Hercules, CA). Rearranged in transformation (RET) antibody was from Neuromics (Edina, MN). Secondary antibodies (Alexa Fluor goat antirabbit 568 and goat antimouse 488) for immunocytochemistry were obtained from MolecularProbes...

New Markers:

Ogg1, Biotinylated
Ogg1, HRP Conjugated

Image: HeLa cells stained with Pin-1 (1:1,000 dilution, green) and fibrillarin (red). Pin-1 stains the nuclear matrix and, much more faintly, the cytoplasm. The fibrillarin antibody marks nucleoli.

Sunday, June 06, 2010

STEMEZ(TM) hNP1 Cells and Neuroprotection Studies

Neuroinflammation has been shown to be a potent negative regulator of stem cell and progenitor cell proliferation in the neurogenic regions of the brain.

Here researchers used our STEMEZ(TM) hNP1 Human Neural Progenitors Expansion Kit to study the neuroprotection capabilities of a propriety nutraceutical formulation.

Adam D. Bachstetter, Jennifer Jernberg, Andrea Schlunk, Jennifer L. Vila, Charles Hudson, Michael J. Cole, R. Douglas Shytle, Jun Tan, Paul R. Sanberg, Cyndy D. Sanberg, Cesario Borlongan, Yuji Kaneko, Naoki Tajiri, Carmelina Gemma, Paula C. Bickford. Spirulina Promotes Stem Cell Genesis and Protects against LPS Induced Declines in Neural Stem Cell Proliferation. PLoS ONE 5(5): e10496. doi:10.1371/journal.pone.0010496.

Abstract:Adult stem cells are present in many tissues including, skin, muscle, adipose, bone marrow, and in the brain. Neuroinflammation has been shown to be a potent negative regulator of stem cell and progenitor cell proliferation in the neurogenic regions of the brain. Recently we demonstrated that decreasing a key neuroinflammatory cytokine IL-1β in the hippocampus of aged rats reversed the age-related cognitive decline and increased neurogenesis in the age rats. We also have found that nutraceuticals have the potential to reduce neuroinflammation, and decrease oxidative stress. The objectives of this study were to determine if spirulina could protect the proliferative potential of hippocampal neural progenitor cells from an acute systemic inflammatory insult of lipopolysaccharide (LPS). To this end, young rats were fed for 30 days a control diet or a diet supplemented with 0.1% spirulina. On day 28 the rats were given a single i.p. injection of LPS (1 mg/kg). The following day the rats were injected with BrdU (50 mg/kg b.i.d. i.p.) and were sacrificed 24 hours after the first injection of BrdU. Quantification of the BrdU positive cells in the subgranular zone of the dentate gyrus demonstrated a decrease in proliferation of the stem/progenitor cells in the hippocampus as a result of the LPS insult. Furthermore, the diet supplemented with spirulina was able to negate the LPS induced decrease in stem/progenitor cell proliferation. In a second set of studies we examined the effects of spirulina either alone or in combination with a proprietary formulation (NT-020) of blueberry, green tea, vitamin D3 and carnosine on the function of bone marrow and CD34+ cells in vitro. Spirulina had small effects on its own and more than additive effects in combination with NT-020 to promote mitochondrial respiration and/or proliferation of these cells in culture. When examined on neural stem cells in culture spirulina increased proliferation at baseline and protected against the negative influence of TNFα to reduce neural stem cell proliferation. These results support the hypothesis that a diet enriched with spirulina and other nutraceuticals may help protect the stem/progenitor cells from insults. Figure 7. Spirulina increases proliferation of human neural stem cells in vitro and protects against a TNFα insult.

Figure: Human neural progenitors grown under proliferation conditions were assessed by MTT assay (A) or BrdU (B) for the effects of spirulina (125 ng/ml) or NT-020 (500 ng/ml) or the two treatments combined in the presence or absence of TNFα (20 ng/ml) for 72 hours. (A) The MTT assay shows that spirulina alone or NT-020 alone increase proliferation; surprising, the in combination proliferation is decrease compare to control ** p less tan 0.005.

Related Reagents:

STEMEZ(TM) hNP1 Human Neural
Progenitors Expansion Kit

Primary Neurons and Astrocytes-Primary
human, rat and mouse neurons and astrocytes

Neuron/Glial Marker Antibodies

Neurotrophins and Growth Factor

Stem Cell Research Reagents
cells, antibodies, proteins, media and FACS kits.

Saturday, May 29, 2010

STEMEZ(TM) hNP1 Human Neural Progenitors and hN2 Primary Neurons Differentiation and Expression

I have received a growing number of requests regarding differentiation and expression patterns of our STEMEZTM cells. This is intended help you gain a clearer understanding. The focus of this document is G-protein Coupled Receptor Expression Patterns. This information was presented by Dr. Steve Stice and his team and the 2008 Neuroscience Conference.


Human embryonic stem cells and their progeny can provide a novel Distribution of detectable transcripts for three cell populations tissue source for understanding developmental pathways, pharmaceutical screening and tissue replacement therapies. G-protein coupled receptors(GPCRs) comprise the largest cell-surface receptor superfamily and are the largest class of drug targets. The study of GPCR signaling in hES cells allows signaling mechanisms to be studied in endogenously expressed receptors in non-transformed cells. We characterized GPCR transcript expression in three cellular populations at different developmental stages: WAO9 human embryonic stem cells, Wa09 derived STEMEZ hNP1 and differentiated hN2 cells maintained 1 week in culture.

Goal: To characterize GPCR transcript expression in human hES cell derived neural tissue

• hES cells displayed the widest array of GPCR transcripts, while neural progenitors displayed the most restricted population.
• The Frizzled (FZD) family of receptors were among the most abundantly expressed transcripts across all populations.
• Neural progentitors up-regulated GPCR transcripts important to brain angiogenesis, cell proliferation, neurogenesis and cell adhesion.
• Further differentiated hN2 cells displayed up-regulation of a wider population of transcripts including GPCRs involved with neurotransmission.
• Functional assays demonstrated responses to sphingosine-1-phosphate in both hNP1 and hN2 populations of cells.
• hES cells and their derived tissue provide a unique model to study endogenous GPCR signaling in non-transformed cells for drug screening applications and to further our understanding of GPCRs role in developmental pathways.

G-protein Coupled Receptor Expression Patterns Are Altered as Human Embryonic Stem Details(pdf - 367Kb). From Poster Presented at Neuroscience 2008 by Dr. Steve Stice et al.

Tuesday, May 25, 2010

Dr. Steve Stice to Present the Power of StemEZ Neural Cells

Dr. Steve Stice to Present the Power of StemEZ Neural Cells

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I have profiled Steve Stice's research here. The focus has been the excellent research results he and his team at ArunA Biomedical have generated with STEMEZ(TM) hN2 Human Neurons and hNP1 Human Neural Progenitors.

The story continues. He will be presenting the latest at the 9th Annual World Pharmaceutical Congress in Philadelphia, June 14. Topics include: using these neural cell lines to study neurotoxicity in cell-based assays and disease modeling. Recent work conducted in outside laboratories demonstrates that these lines are more sensitive to environmental toxicants than traditional cellular models.

Sample high throughput assay applications:

  • Cell morphology and neurite outgrowth

  • Cell signaling and transcription factor expression

  • Receptor and ion channel function

  • Cytotoxicity
  • Apoptosis, genotoxicity and DNA damage

These capabilities has been confirmed by our customers. I look for the use of the STEMEZ cell lines to continue to grow as researchers discover their value in Drug Discovery and Basic Neuroscience capabilities.

Friday, May 21, 2010

Amp up Your Results!

Labeling kits, tags, secondary antibodies and related reagents

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Labeling and tagging is an important step in your research process. This often drives the wow factor in published results. We offer some of the best and brightest including:

CHROMEOTMsity-exhibit superior luminescence properties,
including a broad range of fluorescence excitation and emission, large
Stokes shifts, limited photobleaching and a broad pH tolerance.

ELISA Buffers and Diluents

Solulink™ Labeling Kits and Beads-The most efficient labeling kits delivering ready-to-use conjugates for the novice or the expert!

Cytoplasmic and Nuclear Staining

Strep-Tag®-One-STrEP-tag for protein complex purification.

Image: CHROMEOsity 488: HeLa cells were stained with alpha Tubulin mouse mAb (Clone 5-B-1-2) and Chromeo 488 Goat anti-mouse IgG. The nuclei have been counterstained with DAPI.

Sunday, May 16, 2010

Apoptosis Signaling-Visualization and Measurement.

Apoptosis-Oxidative Stress Research Reagents are widely used and frequently referenced in customer publications. We work hard to keep our fingers on the pulse of how they are utilized across the many research areas important to our customers and add new reagents based on evolving requirements.

I recently posted publications referencing our MitoPTTM Kits for quantitating Tumor Apoptosis

New Pub referencing Polycaspase Assay Kit, green: L. Wei, D. Ding and R. Salvi. Salicylate-induced degeneration of cochlea spiral ganglion neurons-apoptosis signaling.

Images: Typical confocal photomicrographs of SGN stained with Polycaspase Assay Kit (green) and with an antibody against neuronal III ß-tubulin (red) to identify SGN. (A) In control cultures, most SGN have large, oval shaped soma and neurites extending from the soma; note absence of polycaspase labeling (green). (B) SGN treated for 3 h with 5 mM SS; polycaspase labeling was present on SGN with shrunken soma. For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.

Related Reagents:

Polycaspase Assay Kit, green

Magic Red™ Real Time! Kits
-Measure apoptosis in
whole living, intact cells - no lysis required

FLIVO™ Polycaspase Live!, in vivo Apoptosis Kits-New

-Designed for cancer and neurodegenerative disease applications.

FLICA™ in vitro Caspase Kits
-Fast!-Use Caspase
kits to quantitate apoptosis via active caspases in whole, living
cells. These kits do not use ELISA or any antibodies for detection

FLISP™ Serine Protease Detection Kits
chymotrypsin-like protease activation in whole living cells.

MitoPT™ Kits
-Quantitate mitochondrial
functionality and apoptosis