PIM2 report

I. Expression across cell types

II. Expression across tissues

III. Associated gene sets

GO_0008285Biological processnegative regulation of cell population proliferation
GO_0009615Biological processresponse to virus
GO_0016236Biological processmacroautophagy
GO_0008637Biological processapoptotic mitochondrial changes
GO_0043066Biological processnegative regulation of apoptotic process
GO_0045893Biological processpositive regulation of DNA-templated transcription
GO_0016239Biological processpositive regulation of macroautophagy
GO_0043123Biological processpositive regulation of canonical NF-kappaB signal transduction
GO_0010508Biological processpositive regulation of autophagy
GO_0050821Biological processprotein stabilization
GO_0007346Biological processregulation of mitotic cell cycle
GO_0006468Biological processprotein phosphorylation
GO_0046777Biological processprotein autophosphorylation
GO_0000082Biological processG1/S transition of mitotic cell cycle
GO_0005737Cellular componentcytoplasm
GO_0106310Molecular functionprotein serine kinase activity
GO_0004674Molecular functionprotein serine/threonine kinase activity
GO_0005524Molecular functionATP binding
GO_0005515Molecular functionprotein binding

IV. Literature review

[source]
Gene namePIM2
Protein nameSerine/threonine-protein kinase pim-2 (EC 2.7.11.1) (Pim-2h)
non-specific serine/threonine protein kinase (EC 2.7.11.1)
Synonyms
DescriptionFUNCTION: Proto-oncogene with serine/threonine kinase activity involved in cell survival and cell proliferation. Exerts its oncogenic activity through: the regulation of MYC transcriptional activity, the regulation of cell cycle progression, the regulation of cap-dependent protein translation and through survival signaling by phosphorylation of a pro-apoptotic protein, BAD. Phosphorylation of MYC leads to an increase of MYC protein stability and thereby an increase transcriptional activity. The stabilization of MYC exerted by PIM2 might explain partly the strong synergism between these 2 oncogenes in tumorigenesis. Regulates cap-dependent protein translation in a mammalian target of rapamycin complex 1 (mTORC1)-independent manner and in parallel to the PI3K-Akt pathway. Mediates survival signaling through phosphorylation of BAD, which induces release of the anti-apoptotic protein Bcl-X(L)/BCL2L1. Promotes cell survival in response to a variety of proliferative signals via positive regulation of the I-kappa-B kinase/NF-kappa-B cascade; this process requires phosphorylation of MAP3K8/COT. Promotes growth factor-independent proliferation by phosphorylation of cell cycle factors such as CDKN1A and CDKN1B. Involved in the positive regulation of chondrocyte survival and autophagy in the epiphyseal growth plate. .

AccessionsENST00000710069.1
ENST00000710360.1
A0AA34QVH7
Q9P1W9
ENST00000376509.4