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Promotes anchorage-independent cell growth and tumor formation (By similarity). Additionally we are shipping KIAA1524 Antibodies (66) and KIAA1524 Proteins (4) and many more products for this protein.
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Cip2a effectively promotes triple-negative breast cancer (TNBC) cell cycle progression and tumor growth via regulation of PP2A (show PPP2R4 ELISA Kits)/c-myc (show MYC ELISA Kits)/p27Kip1 (show CDKN1B ELISA Kits) signaling, which could serve as a potential therapeutic target for TNBC patients.
poor prognosis of chronic myeloid leukemia (show BCL11A ELISA Kits) patients with high CIP2A levels is due to an antiapoptotic phenotype
Oncoprotein CIP2A is stabilized via interaction with tumor suppressor PP2A/B56
CIP2A is upregulated in MM, and CIP2A expression promotes cell proliferation and clonogenic formation ability by regulating the expression of AKT (show AKT1 ELISA Kits) phosphorylation and c-Myc (show MYC ELISA Kits).
Gambogenic acid is a CIP2A inhibitor that interferes with the ubiquitination and destabilization of CIP2A.
Silencing CIP2A enhanced CuB-induced growth inhibition.
CIP2A copy number increase is associated with poor patient survival in human HNSCC.
These results indicate that CIP2A modulates myeloma cell proliferation and apoptosis via PI3K (show PIK3CA ELISA Kits)/AKT (show AKT1 ELISA Kits)/mTOR (show FRAP1 ELISA Kits) signaling and suggest that it can potentially serve as a drug target for the treatment of multiple myeloma.
CIP2A is involved in regulating multidrug resistance of cervical adenocarcinoma.
These results suggest that CIP2A is involved in tumor progression in bladder cancer
Knockdown of CIP2A by stable CIP2A siRNA transfection inhibited MDA-MB-231 cell proliferation, invasion, colony growth in vitro, and xenograft growth and metastasis in vivo of breast cancer in mice.
CIP2A as a hitherto unrecognized mediator of T-cell activation.
Downregulation of CIP2A suppresses cell proliferation and growth of nasopharyngeal carcinoma.
CIP2A strongly interacts with NEK2 during G2/M phase, thereby enhancing NEK2 kinase activity to facilitate centrosome separation in a PP1- and PP2A-independent manner.
Data show that CIP2A expression can be systematically inhibited without severe consequences to normal mouse development and viability may have clinical relevance regarding targeting of oncogenic CIP2A for future cancer therapies.
Loss of CIP2A in Myc (show MYC ELISA Kits)-overexpressing neural progenitor cells significantly reduces the ability of Myc (show MYC ELISA Kits) to increase self-renewal and proliferation.
Promotes anchorage-independent cell growth and tumor formation (By similarity).
protein CIP2A homolog
, CONSTANS interacting protein 2a
, hypothetical protein LOC100216050
, cancerous inhibitor of PP2A
, p90 autoantigen
, protein CIP2A
, p90 autoantigen homolog