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Interacts with phosphorylated C-terminal heptapeptide repeat domain (CTD) of the largest RNA polymerase II subunit POLR2A, and participates in dephosphorylation of the CTD. Additionally we are shipping Regulation of Nuclear Pre-MRNA Domain Containing 1B Proteins (6) and many more products for this protein.
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Mechanistically, CREPT regulated beta-catenin (show CTNNB1 Antibodies)/TCF4 (show TCF4 Antibodies)/cyclin D1 (show CCND1 Antibodies) pathway in BC. In conclusion, the data suggested that miR (show MLXIP Antibodies)-138/CREPT involved BC progression, providing potential therapeutic targets for BC.
Consistently, samples from oral squamous cell carcinoma (OSCC) patients exhibited a noticeably stronger CREPT expression than noncancerous samples. In contrast, knocking down of CREPT in OSCC cell lines significantly reduced proliferation, colony formation and migration as well as the expression of cyclin D1 (show CCND1 Antibodies) and c-Myc (show MYC Antibodies), but promoted apoptosis.
In addition, CREPT overexpression significantly promoted tumor growth in vivo. Mechanism study showed that CREPT may regulate cell proliferation and cell cycle through the regulation on cyclin D3 (show CCND3 Antibodies), CDK4 (show CDK4 Antibodies) and CDK6 (show CDK6 Antibodies).
a detailed description of proteins associating with K-H/RPRD1B in higher-order protein complexes is required to further elucidate its role in various cellular processes
CREPT displays unique immunostaining for retroperitoneal leiomyosarcoma tissue and can be used to supplement other currently available markers.
study suggests that CREPT acts as an activator to promote transcriptional activity of the beta-catenin.TCF4 complex in response to Wnt (show WNT2 Antibodies) signaling.
RPRD1A (show RPRD1A Antibodies) and RPRD1B associate directly with RPAP2 (show RPAP2 Antibodies) phosphatase and coordinate the dephosphorylation of RNAPII phospho-S5 by RPAP2 (show RPAP2 Antibodies).
RPRD1B overexpression promotes tumor growth and accelerates cell cycle progression.
This study reports that K-H functions in RNAPII regulation, and aids in stabilizing interactions between transcription termination factors, localizing Xrn2 (show XRN2 Antibodies) to the 3'-end of genes and ultimately suppressing R-loop formation.
CREPT increases cyclin D1 (show CCND1 Antibodies) transcription during tumorigenesis.
Interacts with phosphorylated C-terminal heptapeptide repeat domain (CTD) of the largest RNA polymerase II subunit POLR2A, and participates in dephosphorylation of the CTD. Transcriptional regulator which enhances expression of CCND1. Promotes binding of RNA polymerase II to the CCDN1 promoter and to the termination region before the poly-A site but decreases its binding after the poly-A site. Prevents RNA polymerase II from reading through the 3' end termination site and may allow it to be recruited back to the promoter through promotion of the formation of a chromatin loop. Also enhances the transcription of a number of other cell cycle-related genes including CDK2, CDK4, CDK6 and cyclin-E but not CDKN1A, CDKN1B or cyclin-A. Promotes cell proliferation (By similarity).
regulation of nuclear pre-mRNA domain-containing protein 1B
, unm hi3400
, un-named hi3400
, regulation of nuclear pre-mRNA domain containing 1B
, regulation of nuclear pre-mRNA domain containing 1B a
, Regulation of nuclear pre-mRNA domain containing 1B
, cell cycle-related and expression-elevated protein in tumor
, cell-cycle related and expression-elevated protein in tumor