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RBM10 encodes a nuclear protein that belongs to a family proteins that contain an RNA-binding motif. Additionally we are shipping RBM10 Proteins (4) and many more products for this protein.
Showing 10 out of 41 products:
Human Polyclonal RBM10 Primary Antibody for EIA, WB - ABIN954474
Johnston, Teer, Cherukuri, Hansen, Loftus, Chong, Mullikin, Biesecker: Massively parallel sequencing of exons on the X chromosome identifies RBM10 as the gene that causes a syndromic form of cleft palate. in American journal of human genetics 2010
Show all 3 references for ABIN954474
Dog (Canine) Polyclonal RBM10 Primary Antibody for IHC, WB - ABIN2779275
Thiselton, McDowall, Brandau, Ramser, dEsposito, Bhattacharya, Ross, Hardcastle, Meindl: An integrated, functionally annotated gene map of the DXS8026-ELK1 interval on human Xp11.3-Xp11.23: potential hotspot for neurogenetic disorders. in Genomics 2002
Human Polyclonal RBM10 Primary Antibody for ICC, IF - ABIN4349575
Jackson, Du, Janesko-Feldman, Vagni, Dezfulian, Poloyac, Jackson, Clark, Kochanek: The nuclear splicing factor RNA binding motif 5 promotes caspase activation in human neuronal cells, and increases after traumatic brain injury in mice. in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 2015
Src (show SRC Antibodies) family tyrosine kinase (show TXK Antibodies) signaling may regulate FilGAP (show ARHGAP24 Antibodies) through association with RBM10
The ability of RBM10v1 to regulate alternative splicing depends, at least in part, on a structural alteration within the second RNA recognition motif domain, and correlates with preferential expression of the NUMB (show NUMB Antibodies) exon 11 inclusion variant.
RBM10 regulates alternative splicing of Fas (show FAS Antibodies) and Bcl-x (show BCL2L1 Antibodies) genes.
Antagonizes the effects of RBM5 (show RBM5 Antibodies), RBM6 (show RBM6 Antibodies), and RBM10 in cell colony formation.
This study established RBM10 as an important regulator of alternative splicing, presented a mechanistic model for RBM10-mediated splicing regulation and provided a molecular link to understanding a human congenital disorder.
S1-1 contains multiple nuclear localisation sequence that act cooperatively.
Massively parallel sequencing of exons on the X chromosome identifies RBM10 as the gene that causes a syndromic form of cleft palate.
From these results, it seems that the X-chromosome, through its RBM (show RBMY1A1 Antibodies) genes, plays a formerly unknown role in the regulation of programmed cell death (apoptosis) in breast cancer.
S1-1 constitutes hundreds of nuclear domains, which dynamically change their structures in a reversible manner; upon globally reducing RNA polymerase II transcription, S1-1 nuclear bodies enlarge and decrease in number.
results indicate that very few genes are involved in the last steps of the apoptotic cascade in breast cancer, among them one of the X-chromosome RBM (show RBMY1A1 Antibodies) family
Expression of Rbm5 (show RBM5 Antibodies) and Rbm10 RNA remained constant during C2C12 myogenesis, but protein levels significantly decreased.
This gene encodes a nuclear protein that belongs to a family proteins that contain an RNA-binding motif. The encoded protein associates with hnRNP proteins and may be involved in regulating alternative splicing. Defects in this gene are the cause of the X-linked recessive disorder, TARP syndrome. Alternate splicing results in multiple transcript variants.
RNA binding motif protein 10
, RNA-binding protein 10-like
, RNA-binding protein 10
, RNA-binding protein S1-1
, g patch domain-containing protein 9
, RNA-binding motif protein 10
, S1-1 protein from liver