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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.
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 (show MLXIP Proteins)-181a mediated inhibition of cancer susceptibility 2 (CASC2) expression in lung cancer. Results show RNPC1 inhibits NSCLC progression in a miR (show MLXIP Proteins)-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 (show MYC Proteins) expression, which in turn suppresses RBM38 expression. Thus, it can be concluded that RBM38 and c-Myc (show MYC Proteins) form a unique mutually antagonistic RBM38-c-Myc (show MYC Proteins) loop in breast cancer.
Here we uncovered a novel mechanism that RBM38 is a positive posttranscriptional regulator of ZO-1 (show TJP1 Proteins) in breast cancer.
Overexpression of RNA-binding region-containing protein 1 (RNPC1) increased, whereas knockdown of RNPC1 decreased, the level of progesterone receptor (PR (show PGR Proteins)) protein and transcripts.
aplan-Meier analysis showed that renal cell carcinoma (show MOK Proteins) 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 (show MOK Proteins), which has the potential value for the prediction of renal cell carcinoma (show MOK Proteins) prognosis.
RBM38 and DND1 (show DND1 Proteins) are repressed in primary acute myeloid leukemia (show BCL11A Proteins), neutrophil differentiation is dependent on increased expression of both proteins, and they have a role in regulating p21(CIP1 (show CDKN1A Proteins)) expression during acute promyelocytic leukemia (show PML Proteins) 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 (show HIF1A Proteins) under a hypoxic condition.
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 (show TP53 Proteins) via enhanced p53 (show TP53 Proteins) expression.
knockdown of MIC-1 (show GDF15 Proteins) can decrease RNPC1-induced cell growth suppression.
knockdown of p73 (show ARHGAP24 Proteins) or p21, another target of RNPC1, attenuates the inhibitory effect of RNPC1 on cell proliferation and premature senescence, whereas combined knockdown of p73 (show ARHGAP24 Proteins) and p21 completely abolishes it
a novel mechanism by which HuR (show ELAVL1 Proteins) is regulated by RNPC1 via mRNA stability and HuR (show ELAVL1 Proteins) is a mediator of RNPC1-induced growth suppression.
loss of RNPC1 in mouse embryonic fibroblasts increased the level of p53 (show TP53 Proteins) protein, leading to enhanced premature senescence in a p53 (show TP53 Proteins)-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