Ignet

Gene Information

Gene symbol: CDK2

Gene name: cyclin-dependent kinase 2

HGNC ID: 1771

Related Genes

#	Gene Symbol	Number of hits
1	AKT1	1 hits
2	BCL2A1	1 hits
3	CASP2	1 hits
4	CASP8	1 hits
5	CAST	1 hits
6	CCL4	1 hits
7	CCNK	1 hits
8	CDC2	1 hits
9	CDK4	1 hits
10	CDK6	1 hits
11	CDKN1A	1 hits
12	CDKN2A	1 hits
13	CDKN2C	1 hits
14	CFLAR	1 hits
15	GADD45B	1 hits
16	IL1B	1 hits
17	KLRG1	1 hits
18	NFKB1	1 hits
19	NFKB2	1 hits
20	PIM2	1 hits
21	PSMD9	1 hits
22	RELA	1 hits
23	SOD2	1 hits
24	TNFAIP3	1 hits
25	TNFRSF10C	1 hits
26	TNFRSF10D	1 hits
27	TNFSF10	1 hits
28	VEGFA	1 hits
29	XIAP	1 hits

Related Sentences

#	PMID	Sentence
1	22986450	Specific targets in this category included genes asso-ciated with the intrinsic and extrinsic apoptotic pathways (CFLAR, TNFAIP3, TNFRSF10D, SOD2, BCL2A1, BIRC4, PIM2, TNFSF10, TNFRSF10C, CASP2 and CASP8) and genes that act via the NFĸB pathway and other mechanisms to prolong cell viability (NFKB1, NFKB2 and RELA, IL1B, CAST, CDK2,GADD45B, BCL3, BIRC3, CDK2, IL1A, PBEF1, IL6, CXCL1, CCL4 and VEGF).
2	22986450	Moreover, we demonstrate that the X-linked inhibitor of apoptosis protein remained abundant in polymorphonuclear leukocytes over 48 h of LVS infection, whereas BAX mRNA and protein were progressively downregulated.
3	22997239	Dual suppression of the cyclin-dependent kinase inhibitors CDKN2C and CDKN1A in human melanoma.
4	22997239	To identify downstream effectors of MAPK signaling that could be used as potential additional therapeutic targets for BRAF(V600E) inhibitors, we used hTERT/CDK4R24C/p53DD-immortalized primary human melanocytes genetically modified to ectopically express BRAF ( V600E ) or NRAS ( G12D ) and observed induction of the AP-1 transcription factor family member c-Jun.
5	22997239	Using a dominant negative approach, in vitro cell proliferation assays, western blots, and flow cytometry showed that MAPK signaling via BRAF(V600E) promotes melanoma cell proliferation at G1 through AP-1-mediated negative regulation of the INK4 family member, cyclin-dependent kinase inhibitor 2C (CDKN2C), and the CIP/KIP family member, cyclin-dependent kinase inhibitor 1A (CDKN1A).
6	22997239	These effects were antagonized by pharmacological inhibition of CDKN2C and CDKN1A targets CDK2 and CDK4 in vitro.
7	22997239	In contrast to BRAF ( V600E ) or NRAS ( G12D )-expressing melanocytes, melanoma cells have an inherent resistance to suppression of AP-1 activity by BRAF(V600E)- or MEK-inhibitors.
8	24337749	KLRG1 impairs CD4+ T cell responses via p16ink4a and p27kip1 pathways: role in hepatitis B vaccine failure in individuals with hepatitis C virus infection.
9	24337749	In this study, we investigated the expression and function of an inhibitory receptor, killer cell lectin-like receptor subfamily G member 1 (KLRG1), in the regulation of CD4(+) T cells and HBV vaccine responses during HCV infection.
10	24337749	We demonstrated that KLRG1 was overexpressed on CD4(+) T cells from HCV-infected, HBV vaccine nonresponders compared with HBV vaccine responders.
11	24337749	The capacity of CD4(+) T cells to proliferate and secrete IL-2 cytokine was inversely associated with the level of KLRG1 expression.
12	24337749	Importantly, blocking KLRG1 signaling resulted in a significant improvement in CD4(+) T cell proliferation and IL-2 production in HCV-infected, HBV vaccine nonresponders in response to TCR stimulation.
13	24337749	Moreover, blockade of KLRG1 increased the phosphorylation of Akt (Ser(473)) and decreased the expression of cell cycle inhibitors p16(ink4a) and p27(kip1), which subsequently enhanced the expression of cyclin-dependent kinase 2 and cyclin E.
14	24337749	These results suggest that the KLRG1 pathway impairs CD4(+) T cell responses to neoantigen and induces a state of immune senescence in individuals with HCV infection, raising the possibility that blocking this negative-signaling pathway might improve HBV vaccine responses in the setting of chronic viral infection.
15	24695529	However, we show that the KSHV v-cyclin (K-cyclin), which utilizes different CDK partners (CDK4 and CDK6) than the MHV68 v-cyclin (CDK2 and CDC2), can partially rescue the replication defect observed with a v-cyclin null mutant--both in vitro and in vivo.