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1. Chrestensen, C.A., Shuman, J.K., Eschenroeder, A., Worthington, M., Gram, H. and Sturgill, T.W. (2007) MNK1 and MNK2 regulation in HER2-overexpressing breast cancer lines. J. Biol. Chem. 282 , 4243–4252 .
  Notes: These authors investigated the regulation and function of MAPK-interacting protein kinases 1 and 2 (MNK 1 and 2) and other proteins involved in the MAPK pathway in a panel of breast cancer cells. They use an anti-phospho-ERK antibody produced by Promega against a proprietary immunogen to examine the activation status and amounts of ERKs by Western blot analysis. (0003609)
 
 
2. Budinger, G.R.S., Mutlu, G.M., Eisenbart, J., Fuller, A.C., Bellmeyer, A.A., Baker, C.M., Wilson, M., Ridge, K., Barrett, T.A., Lee, V.Y. and Chandel, N.S. (2006) Proapoptotic Bid is required for pulmonary fibrosis. Proc. Natl. Acad. Sci. U S A 103 , 4604-4609 .
  Notes: The authors of this study investigated the role of the mitochondrial-dependent cell death pathway in the development of pulmonary fibrosis after lung injury in a mouse model. The TGFβ1 Emax ImmunoAssay System was used to measure TGFβ1 levels in brochoalveolar lavage fluid from Bid-/- and wildtype mice 5 days after lung injury induced by bleomycin treatment. Mice lacking Bid were protected from pulmonary fibrosis, even although they had similar levels of lung injury, inflammation, and TGFβ1 as wildtype mice 5 days after bleomycin administration. These results indicated that lack of Bid protected against TGFβ1-induced cell death. (0003471)
 
  Products: TGFβ1 Emax® ImmunoAssay System
3. Raffetto, J.D., Vasquez, R., Goodwin, D.G. and Menzoian, J.O. (2006) Mitogen-activated protein kinase pathway regulates cell proliferation in venous ulcer fibroblasts. Vascular and Endovascular Surgery 40 , 59-66 .
  Notes: This study investigates the role of the ERK1/ERK2 (MAPK) pathway in growth regulation of venous ulcer fibroblasts. Human normal (n-fb) and venous ulcer (w-fb) fibroblasts were isolated and grown in culture in the presence or absence of the MEK-1 inhibitor PD 98059. AntiACTIVE® MAPK pAb was used in immunoblots to determine the expression of phosphorylated ERK1/ERK2 in n-fb and w-fb. In separate experiments, human neonatal foreskin fibroblasts were obtained and cultured in the presence of wound fluid from venous ulcers plus or minus PD 98059 to determine whether or not wound fluid had an inhibitory effect on expression of MAPK ERK1/2. Immunoblot analysis using AntiACTIVE® MAPK pAb indicated that wound fluid decreased phosphorylated ERK1/ERK2 expression; addition of PD 98059 did not further decrease expression of phosphorylated ERK1/ERK2 in these cells. (0003537)
 
  Products: Anti-ACTIVE® MAPK pAb, Rabbit, (pTEpY) | PD 98059
4. Borrell-Pages, M., Canals, J.M., Cordelieres, F.P., Parker, J.A., Pineda, J.R., Grange, G., Bryson, E.A., Guillermier, M., Hirsch, E., Hantraye, P., Cheetham, M.E., Neri, C., Alberch, J., Brouillet, E., Saudou, F., and Humbert, S. (2006) Cystamine and cysteamine increase brain levels of BDNF in Huntington disease via HSJ1b and transglutaminase. J. Clin. Invest. 116 , 1410-1424 .
  Notes: This study showed that the heat-shock DnaJ-containing protein 1b (HSJ1b) and cystamine are neuroprotective in Huntington disease and act by increasing release of brain-derived neurotrophic factor (BDNF), which is critical for the survival of striatal neurons. Mouse neuronal cells were transfected with vectors expressing BDNF, HSJ1b, or with a negative control (empty) vector. HSJ1b was shown to significantly increase BDNF release. Treatment of cells with cystamine, a candidate drug for treatment of Huntington disease, also increased BDNF release. RNA interference experiments showed that in cells where HSJ1b expression was reduced, cystamine no longer stimulated BDNF release, indicating that HSJ1b was required for the protective effect mediated by cystamine. In all these experiments the amount of BDNF in the cultured cell supernatants was measured using the BDNF Emax® ImmunoAssay System. (0003480)
 
  Products: BDNF Emax® ImmunoAssay System
5. Hu, D., Serrano, F., Oury, T.D. and Klann, E. (2006) Aging-Dependent alterations in synaptic plasticity and memory in mice that overexpress extracellular superoxide dismutase J. Neuroscience 26 , 3993–3941 .
  Notes: Reactive oxygen species (ROS) are considered neurotoxic and contribute to age-related cognitive decline; however, ROS are also required components of the signal transduction pathways involved in synaptic plasticity and memory. The authors of this study investigated the effect of overexpression of extracellular superoxide dismutase (EC-SOD) in mice. They specifically looked at the activation of stress-related signaling pathways involving ERK, JNK and p38. The AntiACTIVE® MAPK pAb and the Anti-ERK 1/2 pAb were used to probe Western blots of protein isolated from aged wildtype and transgenic mice. The transgenic mice did not show the same age-related upregulation of these proteins as the wildtype mice. (0003671)
 
  Products: Anti-ACTIVE® MAPK Family Sampler | Anti-ERK 1/2 pAb, Rabbit
6. Zha, X-m., Wemmie, J.A., Green, S.H. and Welsh, M.J. (2006) Acid-sensing ion channel 1a is a postsynaptic proton receptor that affects the density of dendritic spines. Proc. Natl. Acad. Sci. USA 103 , 16556-16561 .
  Notes: Acidification can occur during synaptic nerve impulse transmission when the synaptic vesicles empty their contents into the synapse. The authors of this study investigated the role of protons in ion channel regulation at the synapse. They identified the acid-sensing ion channel 1a (ASIC1a) as a proton receptor, and they investigated its relationship to activation of the Ca2+/calmodulin-dependent protein kinase (CaM KII). Anti-ACTIVE® CaM KII pAb was used for Western analysis of immunoprecipitated CaM KII from wildtype or ASIC1a-knockout mouse brains. (0003549)
 
  Products: Anti-ACTIVE® CaM KII pAb, Rabbit, (pT286)
7. Dhandapani, K.M., Wade, F., Mahesh, V.B., and Brann, D (2005) Astrocyte-derived transforming growth factor-β mediates the neuroprotective effects of 17β-estradiol: Involvement of nonclassical genomic signaling pathways. Endocrinology 146 , 2749-2759 .
  Notes: This study investigated the signaling mechanisms involved in 17β-estradiol- (E2) and tamoxifen-induced release of neurotrophic factors from rat cortical astrocyte cultures. The TGFβ1, TGFβ2, BDNF and GDNF Emax® ImmunoAssay Systems were used to measure the release of these neurotrophic factors from astrocyte cultures treated with E2 or tamoxifen. Both E2 and tamoxifen induced the release of TGFβ1 and TGFβ2, but did not stimulate release of BDNF or GDNF. The PI3K inhibitors LY294002 and wortmanin, and the Akt inhibitor blocked TGFβ release, suggesting the involvement of the PI3K/Akt signaling pathway. The MAPK kinase inhibitors PD98059 and U0126 had no effect. E2 was found to induce transient Akt Ser473 phosphorylation, and this effect was blocked by LY294002 pretreatment, demonstrating a role for PI3K in the observed E2-mediated Akt phosphorylation. (0003479)
 
  Products: LY 294002 | PD 98059 | TGFβ Sample 10X Buffer | TGFβ1 Emax® ImmunoAssay System | TGFβ2 Emax® ImmunoAssay System
8. Yang, Y.M., Huang, D.Y., Liu, G.F., Zhong, J.C., Du, K., Li, Y.F. and Song. X.H. (2005) Inhibitory effects of vitamin A on TCDD-induced cytochrome P-450 1A1 enzyme activity and expression. Toxicol. Sci. 85 , 727-734 .
  Notes: The ability of the environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) to upregulate cytochrome P450 CYP1A1 levels in mouse liver was examined. Total mouse liver RNA was reverse transcribed using the Reverse Transcription System, and the resulting CYP1A1 cDNA was quantitated using real-time PCR. CYP1A1 protein levels were quantitated by Western blot using an anti-CYP1A1 antibody, the Anti-Rabbit IgG (Fc), Alkaline Phosphatase Conjugate secondary antibody and the Western Blue® Stabilized Substrate for Alkaline Phosphatase.
(0003443)
 
  Products: Anti-Rabbit IgG (Fc), AP Conjugate | Reverse Transcription System | Western Blue® Stabilized Substrate for Alkaline Phosphatase
9. An, H., Xu, H., Zhang, M., Zhou, J., Feng, T., Qian, C., Qi, R. and Cao, X. (2005) Src homology 2 domain-containing inositol-5-phosphatase 1 (SHIP1) negatively regulates TLR4-mediated LPS response primarily through a phosphatase activity- and PI-3K-independent mechanism. Blood 105 , 4685-4692 .
  Notes: The authors of this study investigated the role of Src homology 2 (SH2) domain-containing inositol-5-phosphatase 1 (SHIP1) in Toll-like receptor 4 (TLR4)-mediated lipopolysaccharide (LPS) response. RAW264.7 macrophages were transfected with wildtype or mutant SHIP1 or control plasmid. Anti-ACTIVE® JNK and p38 antibodies were used in Western analyses to determine phosphorylation of these kinases in response to overexpression of SHIP1 or mutant SHIP1. To investigate any effects on IκB-alpha and NF-κB expression, RAW264.7 macrophages were cotransfected with pGL3-XκB-luciferase reporter plasmid and pRL-TK Renilla luciferase control plasmid. Transfected cells were treated with LPS for 6 hours or left untreated (control). The Dual-Luciferase® Reporter Assay System was used to monitor reporter gene expression. (0003524)
 
  Products: Anti-ACTIVE® JNK pAb, Rabbit, (pTPpY) | Anti-ACTIVE® p38 pAb, Rabbit, (pTGpY) | Dual-Luciferase® Reporter Assay System | Dual-Luciferase® Reporter Assay System 10-Pack | pGL3-Basic Vector | pRL-TK Vector
10. Je, H-S., Zhou, J., Yang, F., and Lu, B. (2005) Distinct mechanisms for neurotrophin-3-induced acute and long-term synaptic potentiation. J. Neurosci. 25 , 11719-11729 .
  Notes: This study investigated the mechanisms of acute and long-term synaptic modulation by neurotrophin-3 (NT-3). The investigators used the Xenopus neuromuscular junction synapse as a model system in which to characterize the effects of short- and long-term exposure to NT-3. Three features were found to be required for long-term, but not acute, effects: 1) endocytosis of the NT-3-receptor complex, 2) Akt activation, and, 3) new protein synthesis. As part of the investigation biotinylated NT-3 was supplied to cultures on streptavidin-coated beads, which were too large to be internalized by endocytosis. In this experiment long-term effects were eliminated but acute effects were unchanged, supporting the requirement for endocytosis of NT-3 for long-term effects. To confirm that NT-3 was tightly bound to the beads, the NT-3-coated beads were vortexed for 30 seconds, and the supernatant collected by centrifugation (5 minutes) and assayed for NT-3 content using the NT-3 Emax® ImmunoAssay System. (0003501)
 
  Products: NT-3 Emax® ImmunoAssay System
11. Munoz, J.R., Stoutenger, B.R., Robinson, A.P., Spees, J.L. and Prockrop, D.J. (2005) Human stem/progenitor cells from bone marrow promote neurogenesis of endogenous neural stem cells in the hippocampus of mice. Proc. Natl. Acad. Sci. U S A 102 , 18171-18176 .
  Notes: In this study, implantation of human bone marrow stem/progenitor cells (MSCs) into the hippocampus of immunodeficient mice was found to stimulate proliferation, migration and differentiation of endogenous neural stem cells. Results of immunohistochemical analyses were confirmed by ELISA. The NGF Emax® Immunoassay System was used to determine NGF levels in isolated hippocampi at various intervals after implantation of the MSCs. (0003500)
 
  Products: NGF Emax® ImmunoAssay System
12. Wang, B., Jenkins, J.R., and Trayhurn, P. (2005) Expression and secretion of inflammation-related adipokines by human adipocytes differentiated in culture: integrated response to TNFα. Am. J. Endocrinol. Metab. 288 , E731-E740 .
  Notes: In this study, the expression of various adipokine genes linked to inflammation was examined during differentiation of pre-adipocytes to adipocytes in primary culture. The effect of TNFα on expression of these adipokines in differentiated human adipocytes was also investigated. qPCR was used to measure expression levels of the various adipokines, including NGF, during development and upon TNFα exposure. In addition, secretion of adipokines into the culture media was measured by ELISA, the NGF Emax® ImmunoAssay System being used to determine NGF levels. (0003502)
 
  Products: NGF Emax® ImmunoAssay System
13. Villadiego, J., Mendez-Ferrer, S., Valdes-Sanchez, T., Silos-Santiago, I., Farinas, I., Lopez-Barneo, J., and Toledo-Aral, J.J. (2005) Selective glial cell line-derived neurotrophic factor production in adult dopaminergic carotid body cells in situ and after intrastrial transplantation. J. Neurosci. 25 , 4091-4098 .
  Notes: In this study, the GDNF Emax® ImmunoAssay System was used to determine the GDNF content of various tissues used to treat Parkinson disease in animals and humans. Tissues tested included rodent carotid body, superior cervical ganglia, adrenal medulla and Zuckerkandl's organs. Tissues were frozen in liquid nitrogen, then homogenized. The ELISA was then performed according to the supplied protocol, with the following exceptions: the anti-GDNF mAb was used at a 1:500 dilution, and the anti-GDNF pAb was used at a 1:250 dilution. GDNF secreted from dissociated cells of the various tissue types was also evaluated in an in situ ELISA, where dissociated cells were cultured for 48 hours in plates coated with anti-GDNF mAb. The cells were then removed by washing and the amount of released GDNF evaluated by ELISA. (0003475)
 
  Products: GDNF Emax® ImmunoAssay System
14. Murakami, A., Shigemori, T. and Ohigashi, H. (2005) Zingiberaceous and citrus constituents, 1'-acetoxychavicol acetate, zerumbone, auraptene, and nobiletin, suppress lipopolysaccharide-induced cyclooxygenase-2 expression in RAW264.7 murine macrophages through different modes of action. J. Nutr. 135 , 2987S-2992S .
  Notes: These authors investigated the mechanisms by which anti-carcinogenic compounds derived from Japanese and subtropical vegetables and fruits attenuate LPS-induced COX-2 mRNA expression in RAW264.7 mouse macrophages. Using Western blot analysis, 10µg nuclear or 20µg cytosolic protein fractions isolated from LPS-treated macrophages in the absence or presence of various phytochemicals were stained with several antibodies for signal pathway proteins, including the Anti-ERK1/2 pAb. Further analysis of the MAPK and NF-κB systems was performed using firefly luciferase constructs co-transfected with the control pRL-TK Vector at a 1:1 ratio. Transfected cells were exposed to the plant compound for 12 hours and then to LPS for a further 12 hours. Reporter activity was measured using the Dual-Luciferase® Reporter Assay System. To determine the effect of the phytochemical zerumbone on the kinase reaction, a cell-free kinase assay was performed using Kinase-Glo® Assay System. In this assay, 1.5µl recombinant MAPKAPK-2, 0.2µl recombinant active p38α, 1µl zerumbone and 4µmol/l ATP were incubated for 3 hours at 28°C before addition of an equal volume of Kinase-Glo® Reagent. (0003333)
 
  Products: Anti-ERK 1/2 pAb, Rabbit | Dual-Luciferase® Reporter Assay System | Dual-Luciferase® Reporter Assay System 10-Pack | Kinase-Glo® Luminescent Kinase Assay | pRL-TK Vector
15. Yang, X., Janatova, J. and Andrade, J.D. (2005) Homogeneous enzyme immunoassay modified for application to luminescence-based biosensors. Anal. Biochem. 336 , 102–107 .
  Notes: CEDIA assays (cloned enzyme donor immunoassays) utilize antibodies to specific analytes that can also bind one of the two beta-galactosidase fragments. The beta-galactosidase fragments can associate with each other provided that the fragment bound to the analyte is not immunoabsorbed, thus blocking the fragment interaction.  The Beta-Glo® Assay System was compared to colorimetric and chemiluminescent detection systems for use in a CEDIA assay with valporic acid as analyte. The Beta-Glo® Assay System gave the best performance in this assay system.  (0003224)
 
  Products: Beta-Glo® Assay System
16. Kermani, P., Rafil, D., Jin, D.K., Whitlock, P., Schaffer, W., Chiang, A., Vincent, L., Friedrich, M., Shido, K., Hackett, N.R., Crystal, R.G., Rafil, S., and Hempstead, B.L. (2005) Neurotrophins promote revascularization by local recruitment of TrkB+ endothelial cells and systemic mobilization of hematopoietic progenitors. J. Clin. Invest. 115 , 653-663 .
  Notes: This study investigated the angiogenic potential of brain-derived neurotrophic factor (BDNF) in ischemic and non-ischemic tissues of adult mice. As part of this study, recombinant Adenovirus encoding rat BDNF was administered to mice via tail-vein injection, and BDNF levels in plasma were then monitored using the BDNF Emax® ImmunoAssay System. (0003473)
 
  Products: BDNF Emax® ImmunoAssay System
17. Pearse, R.N., Swendeman, S.L., Li, Y., Rafil, D. and Hempstead, B.L. (2005) A neurotrophin axis in myeloma: TrkB and BDNF promote tumor cell survival. Blood 105 , 4429-4435 .
  Notes: In this study, the BDNF Emax® ImmunoAssay System was used to measure BDNF levels in heparinized bone marrow plasma from patients with multiple myeloma (MM) and in control samples. The ELISA analysis was used to establish that BDNF is secreted from primary MM cells in vivo. (0003474)
 
  Products: BDNF Emax® ImmunoAssay System
18. Yeh, A.H., Jeffery, P.L., Duncan, R.P., Herington, A.C. and Chopin, L.K. (2005) Ghrelin and a novel pregroghrelin isoform are highly expressed in prostate cancer and ghrelin activates mitogen-activated protein kinase in prostate cancer. Clin. Can. Res. 11 , 8295-8303 .
  Notes: Serum-starved PC3 and LNCaP prostate cancer cells were treated with various concentrations of ghrelin over a time course. Western blots of cell lysates were probed with Anti-ACTIVE® JNK pAb, Anti-ACTIVE® p38 pAb, Anti-ACTIVE® MAPK pAb and Anti-ERK(1/2) pAb to assess activation of MAPK pathways. (0003434)
 
  Products: Anti-ACTIVE® JNK pAb, Rabbit, (pTPpY) | Anti-ACTIVE® MAPK pAb, Rabbit, (pTEpY) | Anti-ACTIVE® p38 pAb, Rabbit, (pTGpY) | Anti-ERK 1/2 pAb, Rabbit
19. O-Uchi, J., Komukai, K., Kusakari, Y., Obata, T., Hongo, K., Sasaki, H. and Kurihara, S. (2005) α1-Adrenoceptor stimulation potentiates L-type Ca2+ current through Ca2+/calmodulin-dependent PK II (CaMKII) activation in rat ventricular myocytes. Proc. Natl. Acad. Sci. U S A 102 , 9400-9405 .
  Notes: Whole-cell extracts were prepared from rat ventricular myocytes treated with various concentrations of phenylephrine. Activation of CaMKII was assessed by Western analysis using Anti-ACTIVE® CaMKII pAb. Anti-ACTIVE® CaMKII pAb was also used to localize phosphorylated CaMKII by immunofluorescence microscopy of ventricular myocytes. Anti-ACTIVE® CaMKII pAb and 15nm gold-conjugated goat anti-rabbit IgG secondary antibodies were used to perform immunoelectron microscopy of isolated myocytes to further determine the subcellular localization of activated CaMKII. (0003435)
 
  Products: Anti-ACTIVE® CaM KII pAb, Rabbit, (pT286)
20. McGough, N.N., He, D.Y., Logrip, M.L., Jeanblanc, J., Phamluong, K., Luong, K., Kharazia, V., Janak, P.H. and Ron D. (2004) RACK1 and brain-derived neurotrophic factor: a homeostatic pathway that regulates alcohol addiction. J. Neurosci. 24 , 10542-10552 .
  Notes: The authors examine the role of brain-derived neurotrophic factor (BDNF) in alcohol addition. RNA was isolated from primary rat hippocampal neurons cultured in the absence or presence of ethanol. The RNA was reverse transcribed using the Reverse Transcription System, and BDNF and GPDH RNAs were quantitated by fluorescent real-time PCR. BDNF and nerve growth factor (NGF) protein levels were monitored using the BNDF and NGF Emax® ImmunoAssay Systems. (0003441)
 
  Products: BDNF Emax® ImmunoAssay System | NGF Emax® ImmunoAssay System | Reverse Transcription System
21. Peden, C.S., Burger, C., Muzyczka, N. and Mandel, R.J. (2004) Circulating anti-wild-type Adeno-associated Virus Type 2 (AAV2) antibodies inhibit recombinant AAV2 (rAAV2)-mediated, but not rAAV5-mediated, gene transfer in the brain. J. Virol. 78 , 6344-6359 .
  Notes: The GDNF Emax® ImmunoAssay System was used to measure GDNF levels in adenovirus-infected rats.  The researchers describe analyzing GDNF levels in brain lysates from naïve, immunized and nonimmunized rats. Naïve animals displayed GDNF expression after infection with an adenovirus vector that expressed GDNF (rAAV2-GDNF). Data aredisplayed graphically as picograms of GDNF per milligram of brain tissue.  (0003254)
 
  Products: GDNF Emax® ImmunoAssay System
22. Szapacs, M.E., Numis, A.L. and Andrews, A.M. (2004) Late onset loss of hippocampal 5-HT and NE is accompanied by increases in BDNF protein expression in mice co-expressing mutant APP and PS1. Neurobiol. Dis. 16(3) , 572-580 .
  Notes: In this study of factors that may contribute to Familial Alzheimer's disease, transgenic mice expressing mutant amyloid precursor protein and mutant presenilin 1 protein were constructed. The levels and effects of several neurotransmitters and BDNF were evaluated by either HPLC analysis or by immunodetection using the BDNF Emax® ImmunoAssay System. The authors describe a method for extraction of BDNF from mouse brain that gives a recovery rate of approximately 70% compared to 2-5% recovery with the standard procedure as given in the BDNF Emax® ImmunoAssay System protocol.  (0003121)
 
  Products: BDNF Emax® ImmunoAssay System
23. Paroni, G., Mizzau, M., Henderson, C., Del Sal, G., Schneider, C. and Brancolini, C. (2004) Caspase-dependent regulation of histone deacetylase 4 nuclear-cytoplasmic shuttling promotes apoptosis. Mol. Biol. Cell 15 , 1804-2818 .
  Notes: In this study, the Anti-PARP p85 Fragment polyclonal antibody was used to confirm apoptosis in human IMR90 and MCF-7 cells by Western blotting lysates from UV- treated cells. The Anti-Cytochrome c monoclonal antibody was also used to immunocytochemically stain IMR90 cells that were transiently transfected with various mutant histone deacetylase-4 (HDAC4)-expressing constructs. Data from these experiments was expressed as the percent of cells showing cytochrome c staining in the cytosol. The researchers also mention using a TNT® Coupled Reticulocyte Lysate System to express and label various histone deacetylases (HDAC1, HDAC2, HDAC3, HDAC4, HDAC5, and HDAC6). The translation products were then used in in vitro cleavage assays with recombinant caspase-2 or caspase-3. (0003174)
 
  Products: Anti-Cytochrome c mAb | Anti-PARP p85 Fragment pAb
24. Beattie, M.S., Harrington, A.W., Lee, R., Kim, J.Y., Boyce, S.L., Longo, F.M., Bresnahan, J.C., Hempstead, B.L. and Yoon, S.O. (2004) ProNGF induces p75-mediated death of oligodendrocytes following spinal cord injury. Neuron 36 , 375–386 .
  Notes: These authors used Western analysis to monitor levels of pro- and mature forms of BDNF and NT-3 from the center of lesions after mouse spinal cord injury. Promega Anti-Human NT-3 pAb and Anti-Human BDNF pAb were used to monitor the mature forms of these neurotrophic factors. (0003201)
 
  Products: Anti-Human BDNF pAb | Anti-Human NT-3 pAb
25. Hsu, C.Y., Bristow, R., Cha, M.S., Wang, B.G., Ho, C.L., Kurman, R.J., Wang, T.L., Shih, Ie.M. (2004) Characterization of active mitogen-activated protein kinase in ovarian serous carcinomas. Clin. Cancer Res. 10 , 6432-6436 .
  Notes: The Anti-ACTIVE® MAPK polyclonal antibody was used to immunohistochemically stain and type patient ovarian serous carcinomas. The researchers used a 1:500 dilution of the antibody on paraffin fixed tissue sections on tissue microarrays. A secondary peroxidase staining kit was used to complete the immunohistochemical staining.  In these studies, the ovarian serous carcinomas displayed increased MAPK expression and activity. Western blots were also performed on tissue lysates using a 1:3000 dilution of the antibody.  (0003210)
 
  Products: Anti-ACTIVE® MAPK pAb, Rabbit, (pTEpY)
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