|Application ||WB, E|
|Calculated MW||44542 Da|
|Antigen Region||343-372 aa|
|Other Names||Serine/threonine-protein kinase pim-1, Pim1, Pim-1|
|Target/Specificity||This Mouse Pim1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 343-372 amino acids from the C-terminal region of mouse Pim1.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||Mouse Pim1 Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Proto-oncogene with serine/threonine kinase activity involved in cell survival and cell proliferation and thus providing a selective advantage in tumorigenesis. Exerts its oncogenic activity through: the regulation of MYC transcriptional activity, the regulation of cell cycle progression and by phosphorylation and inhibition of proapoptotic proteins (BAD, MAP3K5, FOXO3). Phosphorylation of MYC leads to an increase of MYC protein stability and thereby an increase of transcriptional activity. The stabilization of MYC exerted by PIM1 might explain partly the strong synergism between these two oncogenes in tumorigenesis. Mediates survival signaling through phosphorylation of BAD, which induces release of the anti-apoptotic protein Bcl- X(L)/BCL2L1. Phosphorylation of MAP3K5, an other proapoptotic protein, by PIM1, significantly decreases MAP3K5 kinase activity and inhibits MAP3K5-mediated phosphorylation of JNK and JNK/p38MAPK subsequently reducing caspase-3 activation and cell apoptosis. Stimulates cell cycle progression at the G1-S and G2-M transitions by phosphorylation of CDC25A and CDC25C. Phosphorylation of CDKN1A, a regulator of cell cycle progression at G1, results in the relocation of CDKN1A to the cytoplasm and enhanced CDKN1A protein stability. Promote cell cycle progression and tumorigenesis by down-regulating expression of a regulator of cell cycle progression, CDKN1B, at both transcriptional and post- translational levels. Phosphorylation of CDKN1B,induces 14-3-3 binding, nuclear export and proteasome-dependent degradation. May affect the structure or silencing of chromatin by phosphorylating HP1 gamma/CBX3. Acts also as a regulator of homing and migration of bone marrow cells involving functional interaction with the CXCL12-CXCR4 signaling axis (By similarity).|
|Cellular Location||Cytoplasm. Nucleus. Cell membrane. Note=Mainly located in the cytoplasm|
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Provided below are standard protocols that you may find useful for product applications.
Pim1 may affect the structure or silencing of chromatin by phosphorylating HP1 gamma/CBX3 (By similarity). Promotes the G1/S transition of the cell cycle via up-regulation of CDK2 activity and phosphorylation of CDKN1B, resulting in enhanced nuclear export and proteasome-dependent degradation of CDKN1B (By similarity). Also represses CDKN1B transcription by phosphorylating and inactivating the transcription factor FOXO3 (By similarity). Plays a role in signal transduction in blood cells (By similarity). Contributes to both cell proliferation and survival thus providing a selective advantage in tumorigenesis (By similarity).
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