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Human Polyclonal RBM38 Primary Antibody für WB - ABIN527566
Huang, Jeong, Okamura, Sook-Kim, Zhu, Guerrero-Preston, Ratovitski: Global tumor protein p53/p63 interactome: making a case for cisplatin chemoresistance. in Cell cycle (Georgetown, Tex.) 2012
Cow (Bovine) Polyclonal RBM38 Primary Antibody für WB - ABIN2779112
Shu, Yan, Chen: RNPC1, an RNA-binding protein and a target of the p53 family, is required for maintaining the stability of the basal and stress-induced p21 transcript. in Genes & development 2006
Show all 2 Pubmed References
The data suggested that XSeb4R is a novel player in gene expression regulation, acting at the posttranscriptional level during ectoderm specification in Xenopus.
Has a proneural effect involved in the genetic network of retinogenesis.
Ablation of XSeb4R activity results in impairment of endoderm and mesoderm formation, while ectopic expression of XSeb4R in ectodermal cells induces endodermal and mesodermal gene expression.
results reveal a critical mechanism by which Ser-195 phosphorylation in Rbm38 increases p63 expression by attenuating the association of Rbm38 with the Ago2-miR203 complex.
Study investigates the biological significance of the Rbm38-p63 loop and finds that Rbm38 and p63 function as intergenic suppressors in aging and tumorigenesis.
Our findings suggested that RBM38 may be a core contributor in stabilizing the p53-mdm2 loop function to prevent hepatocellular carcinoma (HCC) and a potential novel target to provide a therapeutic strategy for HCC by inhibiting mdm2 and rescuing p53 from inactivation
Investigated RNA-binding region-containing protein 1 (RNPC1) action on signal pathways and disease progression in lung cancer samples and cells. Found RNPC1 acts to downregulate the miR-181a mediated inhibition of cancer susceptibility 2 (CASC2) expression in lung cancer. Results show RNPC1 inhibits NSCLC progression in a miR-181a/CASC2 axis-dependent manner.
Results showed that the expressions of RBM38 and PTEN was positively correlated in human breast cancer tissues. RBM38 upregulated PTEN expression and activity in breast cancer cells through its direct binding to PTEN mRNA 3'UTR enhancing its stability. These data implied that RBM38 acted as a tumor suppressor partly by enhancing PTEN expression.
Taken together, these results suggest that the 11-kDa protein facilitates B19V DNA replication and that RBM38 is an essential host factor for B19V pre-mRNA splicing and for the expression of the 11-kDa protein.
Results report that RBM38 mediates direct inhibition of c-Myc expression, which in turn suppresses RBM38 expression. Thus, it can be concluded that RBM38 and c-Myc form a unique mutually antagonistic RBM38-c-Myc loop in breast cancer.
Here we uncovered a novel mechanism that RBM38 is a positive posttranscriptional regulator of ZO-1 in breast cancer.
Overexpression of RNA-binding region-containing protein 1 (RNPC1) increased, whereas knockdown of RNPC1 decreased, the level of progesterone receptor (PR) protein and transcripts.
aplan-Meier analysis showed that renal cell carcinoma patients with lower expression of RBM38 had a significantly shorter survival time than those with higher expression of RBM38 ( p = 0.028). All these suggested that RBM38 acts as a tumor suppressor in renal cell carcinoma, which has the potential value for the prediction of renal cell carcinoma prognosis.
RBM38 and DND1 are repressed in primary acute myeloid leukemia, neutrophil differentiation is dependent on increased expression of both proteins, and they have a role in regulating p21(CIP1) expression during acute promyelocytic leukemia differentiation
RNPC1 was found to be expressed in bladder, blood, brain, breast, colorectal, eye, head and neck, lung, ovarian, skin and soft tissue cancer. In 14 of the 94 tests, an association between RNPC1 gene expression and cancer prognosis was observed.
our data suggest that RBM38 is a novel translational regulator of HIF1alpha under a hypoxic condition.
Suggest that RNPC1 had a potential function to play a tumor-suppressor role which may be a potential marker in the therapeutic and prognostic of breast cancer.
Data indicate that long non-coding RNA HOTAIR is functionally related to RNA binding motif protein 38 (RBM38).
RBM38 as novel transcriptional target of E2F1 restricts E2F1-induced proliferation. Furthermore, this negative feedback loop seems to restrict tumor aggressiveness, thereby promoting survival of patients with cancer.
A role for RBM38 in regulating alternative splicing during erythroid differentiation.
Data suggest that RNPC1 is a critical regulator of Mdm2.
GSK3 promotes p53 mRNA translation through phosphorylation of RNPC1
knockdown of MIC-1 can decrease RNPC1-induced cell growth suppression.
The hearts of Rbm38 -/- mice were mildly hypertrophic, but cardiac function was not affected. Furthermore, Rbm38 deficiency did not affect cardiac remodeling (i.e. hypertrophy, LV dilation and fibrosis) or performance (i.e. fractional shortening) after pressure-overload induced by transverse aorta constriction.
Rbm38 deficiency markedly decreases the tumor penetrance in mice heterozygous for p53 via enhanced p53 expression.
knockdown of p73 or p21, another target of RNPC1, attenuates the inhibitory effect of RNPC1 on cell proliferation and premature senescence, whereas combined knockdown of p73 and p21 completely abolishes it
a novel mechanism by which HuR is regulated by RNPC1 via mRNA stability and HuR is a mediator of RNPC1-induced growth suppression.
loss of RNPC1 in mouse embryonic fibroblasts increased the level of p53 protein, leading to enhanced premature senescence in a p53-dependent manner
RNA-binding protein that specifically bind the 3'-UTR of CDKN1A transcripts, leading to maintain the stability of CDKN1A transcripts, thereby acting as a mediator of the p53/TP53 family to regulate CDKN1A. CDKN1A is a cyclin-dependent kinase inhibitor transcriptionally regulated by the p53/TP53 family to induce cell cycle arrest. Has the ability to induce cell cycle arrest in G1 and maintain the stability of CDKN1A transcripts induced by p53/TP53. Also acts as a mRNA splicing factor. Specifically regulates the expression of FGFR2-IIIb, an epithelial cell- specific isoform of FGFR2 (By similarity). Plays a role in myogenic differentiation.
RNA binding motif protein 38
, RNA-binding protein 38
, RNA-binding motif protein 38
, RNA-binding region (RNP1, RRM) containing 1
, RNA-binding region containing 1
, RNA-binding protein XSeb4R
, RRM-type RNA-binding protein XSEB4R
, hypothetical protein
, CLL-associated antigen KW-5
, RNA-binding region-containing protein 1
, ssDNA-binding protein SEB4
, seb4 mRNA