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Promotes anchorage-independent cell growth and tumor formation (By similarity)..
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High expression of CIP2A is associated with cisplatin resistant gastric cancer.
These data reveal that CIP2A is a crucial mediator of FN-induced bladder cancer cell proliferation via enhancing the stabilization of beta-catenin (show CTNNB1 Proteins).
confirmed the high mRNA and protein expression levels of CIP2A in hepatocellular carcinoma (HCC (show FAM126A Proteins)), and found high CIP2A mRNA expression level was associated with unfavorable overall and recurrence-free survival in patients with HCC (show FAM126A Proteins)
High CIP2A expression is associated with gemcitabine resistance in pancreatic cancer.
These results are the first evidence that the inhibition of HDAC1 (show HDAC1 Proteins) by (S)-2 downregulates CIP2A transcription
Membranous CIP2A expression as a potential novel prognostic and predictive indicator for tamoxifen resistance.
Cip2a effectively promotes triple-negative breast cancer (TNBC) cell cycle progression and tumor growth via regulation of PP2A (show PPP2R4 Proteins)/c-myc (show MYC Proteins)/p27Kip1 (show CDKN1B Proteins) signaling, which could serve as a potential therapeutic target for TNBC patients.
poor prognosis of chronic myeloid leukemia (show BCL11A Proteins) patients with high CIP2A levels is due to an antiapoptotic phenotype
Oncoprotein CIP2A is stabilized via interaction with tumor suppressor PP2A (show PPP2R4 Proteins)/B56
CIP2A is upregulated in MM, and CIP2A expression promotes cell proliferation and clonogenic formation ability by regulating the expression of AKT (show AKT1 Proteins) phosphorylation and c-Myc (show MYC Proteins).
CIP2A acts as a scaffold for CEP192-mediated microtubule organizing center assembly by recruiting Plk1 and aurora A (show AURKA Proteins) during meiotic maturation in mouse oocytes
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 (show NEK2 Proteins) during G2/M phase, thereby enhancing NEK2 kinase (show NEK2 Proteins) activity to facilitate centrosome separation in a PP1 (show PPP1CC Proteins)- and PP2A (show PPP2R2B Proteins)-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 Proteins)-overexpressing neural progenitor cells significantly reduces the ability of Myc (show MYC Proteins) to increase self-renewal and proliferation.
Promotes anchorage-independent cell growth and tumor formation (By similarity).
cancerous inhibitor of PP2A
, p90 autoantigen
, protein CIP2A
, p90 autoantigen homolog
, protein CIP2A homolog
, CONSTANS interacting protein 2a
, hypothetical protein LOC100216050