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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

SERTA domain containing 1

SEI-1, TRIP-Br1, TRIP-Br, SEII
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Top mentioned proteins: TRIP, PCNA, TRIP-Br2, CDK4, E2F1
Papers on SEI-1
TRIP-Br1 oncoprotein inhibits autophagy, apoptosis, and necroptosis under nutrient/serum-deprived condition.
New
Lee et al., Seoul, South Korea. In Oncotarget, Nov 2015
TRIP-Br1 oncogenic protein has been shown to have multiple biological functions in cells.
Nutrient/serum starvation derived TRIP-Br3 down-regulation accelerates apoptosis by destabilizing XIAP.
New
Lee et al., Seoul, South Korea. In Oncotarget, May 2015
TRIP-Br3 and TRIP-Br1 have shown to have important biological functions.
KLF10 affects pancreatic function via the SEI-1/p21Cip1 pathway.
New
Chang et al., Taiwan. In Int J Biochem Cell Biol, Mar 2015
Using ChIP-chip screening, SEI-1 was identified as a target gene that may be regulated by KLF10.
Coordinated expression of cyclin-dependent kinase-4 and its regulators in human oral tumors.
Li et al., Columbus, United States. In Anticancer Res, 2014
BACKGROUND/AIM: While aberrant expression of cyclin-dependent kinase-4 (CDK4) has been found in squamous cell carcinoma of the head and neck (SCCHN), the associations between CDK4 and its regulators, namely, cyclin D1, cyclin E, gankyrin, SEI1, and BMI1 in gene expression remain to be explored.
Distinct regulatory effect of the p34SEI-1 oncoprotein on cancer metastasis in HER2/neu-positive and -negative cells.
Lee et al., Seoul, South Korea. In Int J Oncol, 2014
The p34(SEI-1) oncoprotein is involved in a transcriptional regulation, cell cycle regulation, apoptosis, development and many other important cellular functions.
Oncogenic function of p34SEI-1 via NEDD4‑1‑mediated PTEN ubiquitination/degradation and activation of the PI3K/AKT pathway.
Lee et al., Seoul, South Korea. In Int J Oncol, 2013
A 34-KD protein encoded by the SEI-1 gene (p34(SEI‑1)), is a relatively recently discovered oncoprotein that has multiple important biological functions.
Evidence that P12, a specific variant of P16(INK4A), plays a suppressive role in human pancreatic carcinogenesis.
Li et al., Columbus, United States. In Biochem Biophys Res Commun, 2013
In the current study, we demonstrated that over-expression of p12 in human pancreatic cancer cells led to cell arrest at the G1 phase and such cell cycle arrest was related to down-regulation of a number of oncogenes, such as c-Jun, Fos, and SEI1.
p34 (SEI-1) inhibits ROS-induced cell death through suppression of ASK1.
GeneRIF
Lee et al., Seoul, South Korea. In Cancer Biol Ther, 2011
These results suggest that p34 (SEI-1) inhibits ROS-induced cell death through by indirectly inducing ubiquitination of ASK1.
I-mfa domain proteins specifically interact with SERTA domain proteins and repress their transactivating functions.
Eizuru et al., Kagoshima, Japan. In Biochimie, 2011
We show here that I-mfa and HIC specifically interact with SEI-1 through their C-terminal I-mfa domains in vivo.
Effect of PP2A on p34SEI-1 expression in response to ionizing radiation in MCF-7 human breast cancer cells.
GeneRIF
Lee et al., Seoul, South Korea. In Int J Oncol, 2011
study shows that the p34SE1-1 expression level was not changed after H2O2 treatment at either protein or transcriptional levels
Characterization of a novel mechanism of genomic instability involving the SEI1/SET/NM23H1 pathway in esophageal cancers.
GeneRIF
Guan et al., Guangzhou, China. In Cancer Res, 2010
Translocation of small amount of NM23H1 into the nucleus induced by the overexpressions of SEI1/SET could increase the frequency of sister chromatid exchangein esophageal cancers.
Normal proliferation and tumorigenesis but impaired pancreatic function in mice lacking the cell cycle regulator sei1.
Serrano et al., Madrid, Spain. In Plos One, 2009
Sei1 is a positive regulator of proliferation that promotes the assembly of Cdk4-cyclin D complexes and enhances the transcriptional activity of E2f1.
p34SEI-1 inhibits doxorubicin-induced senescence through a pathway mediated by protein kinase C-delta and c-Jun-NH2-kinase 1 activation in human breast cancer MCF7 cells.
Lee et al., Seoul, South Korea. In Mol Cancer Res, 2009
In this study, we describe a novel function of the p34(SEI-1) protein, which is both an oncogenic protein and a positive regulator of the cell cycle.
p34SEI-1 inhibits apoptosis through the stabilization of the X-linked inhibitor of apoptosis protein: p34SEI-1 as a novel target for anti-breast cancer strategies.
Lee et al., Seoul, South Korea. In Cancer Res, 2009
The p34(SEI-1) protein exerts oncogenic effects via regulation of the cell cycle, which occurs through a direct interaction with cyclin-dependent kinase 4. Such regulation can increase the survival of various types of tumor cells.
Identification of PP2A as a novel interactor and regulator of TRIP-Br1.
Hsu et al., Boston, United States. In Cell Signal, 2009
Three of the four mammalian members of TRIP-Br family, including TRIP-Br1, are known oncogenes.
TRIP-Br2 promotes oncogenesis in nude mice and is frequently overexpressed in multiple human tumors.
Hsu et al., Boston, United States. In J Transl Med, 2008
BACKGROUND: Members of the TRIP-Br/SERTAD family of mammalian transcriptional coregulators have recently been implicated in E2F-mediated cell cycle progression and tumorigenesis.
Dissection of CDK4-binding and transactivation activities of p34(SEI-1) and comparison between functions of p34(SEI-1) and p16(INK4A).
GeneRIF
Tsai et al., Columbus, United States. In Biochemistry, 2005
p34(SEI-1) and p16(INK4A) have different roles in development of squamous cell carcinoma of the head and neck
The nuclear protein p34SEI-1 regulates the kinase activity of cyclin-dependent kinase 4 in a concentration-dependent manner.
GeneRIF
Muscarella et al., Columbus, United States. In Biochemistry, 2004
p34SEI1 fragment 30-160 can bind, activate, and inhibit cyclin-dependent kinase CDK4; fragment 30-132 binds and activates but does not inhibit CDK4, while fragment 30-88 cannot bind, activate, or inhibit but retains LexA-mediated transactivation activity.
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