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The data suggested that XSeb4R is a novel player in gene expression regulation, acting at the posttranscriptional level during ectoderm specification in Xenopus.
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 report that RBM38 mediates direct inhibition of c-Myc (zeige MYC ELISA Kits) expression, which in turn suppresses RBM38 expression. Thus, it can be concluded that RBM38 and c-Myc (zeige MYC ELISA Kits) form a unique mutually antagonistic RBM38-c-Myc (zeige MYC ELISA Kits) loop in breast cancer.
Here we uncovered a novel mechanism that RBM38 is a positive posttranscriptional regulator of ZO-1 (zeige TJP1 ELISA Kits) in breast cancer.
Overexpression of RNA-binding region-containing protein 1 (RNPC1) increased, whereas knockdown of RNPC1 decreased, the level of progesterone receptor (PR (zeige PGR ELISA Kits)) 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 (zeige DND1 ELISA Kits) are repressed in primary acute myeloid leukemia (zeige BCL11A ELISA Kits), neutrophil differentiation is dependent on increased expression of both proteins, and they have a role in regulating p21(CIP1 (zeige CDKN1A ELISA Kits)) expression during acute promyelocytic leukemia (zeige PML ELISA Kits) 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 (zeige HIF1A ELISA Kits) 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 (zeige E2F1 ELISA Kits) restricts E2F1 (zeige E2F1 ELISA Kits)-induced proliferation. Furthermore, this negative feedback loop seems to restrict tumor aggressiveness, thereby promoting survival of patients with cancer.
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 (zeige TP53 ELISA Kits) via enhanced p53 (zeige TP53 ELISA Kits) expression.
knockdown of MIC-1 (zeige GDF15 ELISA Kits) can decrease RNPC1-induced cell growth suppression.
knockdown of p73 (zeige ARHGAP24 ELISA Kits) or p21, another target of RNPC1, attenuates the inhibitory effect of RNPC1 on cell proliferation and premature senescence, whereas combined knockdown of p73 (zeige ARHGAP24 ELISA Kits) and p21 completely abolishes it
a novel mechanism by which HuR (zeige ELAVL1 ELISA Kits) is regulated by RNPC1 via mRNA stability and HuR (zeige ELAVL1 ELISA Kits) is a mediator of RNPC1-induced growth suppression.
loss of RNPC1 in mouse embryonic fibroblasts increased the level of p53 (zeige TP53 ELISA Kits) protein, leading to enhanced premature senescence in a p53 (zeige TP53 ELISA Kits)-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