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|Tested species reactivity||Human, Rat|
|Published species reactivity||Mouse, Human|
|Host / Isotype||Rabbit / IgG|
|Immunogen||Synthetic phosphopeptide corresponding to a region surrounding the phosphorylated Thr180/Tyr182 residues of p38 MAP kinase.|
|Storage buffer||0.01M HEPES, pH 7.5, with 0.15M NaCl, 100µg/ml BSA, 50% glycerol|
|Tested Applications||Dilution *|
|Immunohistochemistry (Paraffin) (IHC (P))||1:250|
|Western Blot (WB)||1:1000|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
This antibody is predicted to react with bovine, canine, chicken, mouse, non-human primates and zebrafish based on 100% sequence homology.
The protein encoded by this gene is a member of the MAP kinase family. MAP kinases act as an integration point for multiple biochemical signals, and are involved in a wide variety of cellular processes such as proliferation, differentiation, transcription regulation and development. This kinase is activated by various environmental stresses and proinflammatory cytokines. The activation requires its phosphorylation by MAP kinase kinases, or its autophosphorylation triggered by the interaction of MAP3K7IP1/TAB1 protein with this kinase. The substrates of this kinase include transcription regulator ATF2, MEF2C, and MAX, cell cycle regulator CDC25B, and tumor suppressor p53, which suggest the roles of this kinase in stress related transcription and cell cycle regulation, as well as in genotoxic stress response. Four alternatively spliced transcript variants of this gene encoding distinct isoforms have been reported.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
Opposing effects of membrane-anchored CX3CL1 on amyloid and tau pathologies via the p38 MAPK pathway.
36-8500 was used in western blot to investigate the role of membrane-anchored versus soluble CX3CL1 in regulating the microglia-mediated amelioration of Abeta pathology.
|Lee S,Xu G,Jay TR,Bhatta S,Kim KW,Jung S,Landreth GE,Ransohoff RM,Lamb BT||The Journal of neuroscience : the official journal of the Society for Neuroscience (34:12538)||2014|
Microglial derived tumor necrosis factor-α drives Alzheimer's disease-related neuronal cell cycle events.
36-8500 was used in western blot to investigate the role of microglial derived tumor necrosis factor alpha in neuronal cell cycle progression
|Bhaskar K,Maphis N,Xu G,Varvel NH,Kokiko-Cochran ON,Weick JP,Staugaitis SM,Cardona A,Ransohoff RM,Herrup K,Lamb BT||Neurobiology of disease (62:273)||2014|
|Mouse||Not Cited||Growth-factor receptor-bound protein-2 (Grb2) signaling in B cells controls lymphoid follicle organization and germinal center reaction.||Jang IK,Cronshaw DG,Xie LK,Fang G,Zhang J,Oh H,Fu YX,Gu H,Zou Y||Proceedings of the National Academy of Sciences of the United States of America (108:7926)||2011|
|Human||Not Cited||T-cell receptor ligation induces distinct signaling pathways in naive vs. antigen-experienced T cells.||Adachi K,Davis MM||Proceedings of the National Academy of Sciences of the United States of America (108:1549)||2011|
|Mouse||Not Cited||Cell death or survival promoted by alternative isoforms of ErbB4.||Sundvall M,Veikkolainen V,Kurppa K,Salah Z,Tvorogov D,van Zoelen EJ,Aqeilan R,Elenius K||Molecular biology of the cell (21:4275)||2010|
|Mouse||Not Cited||p38 Mitogen-activated protein kinase plays a stimulatory role in hepatic gluconeogenesis.||Cao W,Collins QF,Becker TC,Robidoux J,Lupo EG,Xiong Y,Daniel KW,Floering L,Collins S||The Journal of biological chemistry (280:42731)||2005|
|Mouse||Not Cited||Selective activation of mitogen-activated protein (MAP) kinase kinase 3 and p38alpha MAP kinase is essential for cyclic AMP-dependent UCP1 expression in adipocytes.||Robidoux J,Cao W,Quan H,Daniel KW,Moukdar F,Bai X,Floering LM,Collins S||Molecular and cellular biology (25:5466)||2005|
||T-cell receptor ligation induces distinct signaling pathways in naive vs. antigen-experienced T cells.||Adachi K,Davis MM||Proceedings of the National Academy of Sciences of the United States of America (108:1549)||2011|
CSAID binding protein; CSAID-binding protein; Csaids binding protein; CSBP1; CSBP2; Cytokine suppressive anti- inflammatory drug binding protein; cytokine suppressive anti-inflammatory drug binding protein; Cytokine suppressive anti-inflammatory drug-binding protein; cytokine-supressive anti-inflammatory drug binding protein; EC 188.8.131.52; MAP kinase 14; MAP kinase 2; MAP kinase MXI2; MAP kinase p38; MAP kinase p38 alpha; MAPK 14; MAPK14; MAX-interacting protein 2; Mitogen-activ; Mitogen-activated protein kinase 14; mitogen-activated protein kinase 14A; Mitogen-activated protein kinase p38 alpha; MK14; MXI2; p38 MAP kinase; p38 mitogen activated protein kinase; p38alpha Exip; reactive kinase; SAPK2a; Stress-activated protein kinase 2a
CRK1; CSBP; CSBP1; CSBP2; CSPB1; EXIP; Hog; MAPK14; MXI2; p38; p38ALPHA; p38Hog; PRKM14; PRKM15; RK; SAPK2A