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MAPK9 Primary Antibody
|Aliases||JNK2; SAPK; p54a; JNK2A; JNK2B; PRKM9; JNK-55; SAPK1a; JNK2BETA; p54aSAPK; JNK2ALPHA|
|Formulation||Purified antibody in PBS with 0.05% sodium azide|
|IHC_P (Immunohistochemistry)||Purified recombinant fragment of human DFFB (AA: 1-289) expressed in E. Coli.|
|FCM (Flow Cytometry)||1/200 - 1/400|
|(AA: 227-382) expressed in E. Coli.|
Figure 1: Black line: Control Antigen (100 ng);Purple line: Antigen (10ng); Blue line: Antigen (50 ng); Red line:Antigen (100 ng)
Figure 2: Western blot analysis using MAPK9 mAb against human MAPK9 (AA: 227-382) recombinant protein. (Expected MW is 44.4 kDa)
Figure 3: Western blot analysis using MAPK9 mAb against HEK293 (1) and MAPK9 (AA: 227-382)-hIgGFc transfected HEK293 (2) cell lysate.
Figure 4: Western blot analysis using MAPK9 mouse mAb against HEK293 (1) and U251 (2) cell lysate.
Figure 5: Flow cytometric analysis of Hela cells using MAPK9 mouse mAb (green) and negative control (red).
|Tissue Array Results|
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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 targets specific transcription factors, and thus mediates immediate-early gene expression in response to various cell stimuli. It is most closely related to MAPK8, both of which are involved in UV radiation induced apoptosis, thought to be related to the cytochrome c-mediated cell death pathway. This gene and MAPK8 are also known as c-Jun N-terminal kinases. This kinase blocks the ubiquitination of tumor suppressor p53, and thus it increases the stability of p53 in nonstressed cells. Studies of this gene's mouse counterpart suggest a key role in T-cell differentiation. Several alternatively spliced transcript variants encoding distinct isoforms have been reported.
|References (references)||1.Neuro Oncol. 2016 Jul;18(7):950-61.
2.Biochem Cell Biol. 2015 Dec;93(6):604-10.