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alternative splicing patterns were altered by knockdown of RBM4 in several types of neoplasms
Loss of RBM4 expression is associated with colorectal cancer.
The results indicate that the alanine-rich C-terminal domain, in conjunction with its conjoined RNA-binding domain(s), differentially influences the subnuclear localization and biogenesis of RBM4.
Up-regulation of RBM4 is associated with breast cancer.
RBM4 is a tumor suppressor with therapeutic potential and clinical values as a prognostic factor.
we propose the emerging role of RBM4 in regulating the adipocyte-specific splicing events and transcription cascade, which subsequently facilitate the development and function of brown adipocyte-like cells.
role in negative feed-forward loop that disrupts inflammattory cytokine translation following Toll-like receptor 4 (show TLR4 Proteins) response
RBM4 homologs exert different effects on 5' splice site utilization and exon selection, and exhibit different subnuclear localization patterns.
RBM4 may synergize its effect on muscle cell-specific alternative splicing by down-regulating PTB (show PTBP1 Proteins) expression and antagonizing the activity of PTB (show PTBP1 Proteins) in exon selection
Data show that RBM4 interacts directly with Ago2 (show EIF2C2 Proteins) during muscle cell differentiation and may recruit Ago2 (show EIF2C2 Proteins) to suppress translation of target mRNAs.
These results constitute a mechanistic understanding of the RBM4a-modulated splicing cascade during the brown adipogenesis.
The RBM4-MEF2C-miR-1 network constitutes a novel mechanism which programs the gene expression profile toward the development of brown adipocytes.
RBM4 overexpression was sufficient to convert AR42J cells into insulin (show INS Proteins)-producing cells and may mediate glucose-induced insulin (show INS Proteins) expression and insulin receptor (show INSR Proteins) isoform switches.
LARK ia a novel posttranscriptional regulator of the mammalian circadian clock.
RNA-binding factor involved in multiple aspects of cellular processes like alternative splicing of pre-mRNA and translation regulation. Modulates alternative 5'-splice site and exon selection. Acts as a muscle cell differentiation-promoting factor. Activates exon skipping of the PTB pre-mRNA during muscle cell differentiation. Antagonizes the activity of the splicing factor PTBP1 to modulate muscle cell-specific exon selection of alpha tropomyosin. Binds to intronic pyrimidine-rich sequence of the TPM1 and MAPT pre-mRNAs. Required for the translational activation of PER1 mRNA in response to circadian clock. Binds directly to the 3'-UTR of the PER1 mRNA. Exerts a suppressive activity on Cap-dependent translation via binding to CU-rich responsive elements within the 3'UTR of mRNAs, a process increased under stress conditions or during myocytes differentiation. Recruits EIF4A1 to stimulate IRES-dependent translation initiation in respons to cellular stress. Associates to internal ribosome entry segment (IRES) in target mRNA species under stress conditions. Plays a role for miRNA-guided RNA cleavage and translation suppression by promoting association of EIF2C2- containing miRNPs with their cognate target mRNAs. Associates with miRNAs during muscle cell differentiation. Binds preferentially to 5'-CGCGCG-3' motif in vitro (By similarity).
RNA binding motif protein 4
, RNA-binding motif protein 4.1
, RNA-binding protein 4.1
, RNA-binding motif protein 4a
, RNA-binding protein 4
, lark homolog
, transcriptional coactivator CoAZ
, zinc finger CCHC-type and RNA binding motif 3A
, RNA-binding motif protein 4