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RAB23, member RAS oncogene family

The protein encoded by this gene belongs to the small GTPase superfamily, Rab family. It may be involved in small GTPase mediated signal transduction and intracellular protein transportation. Alternative splicing occurs at this locus and two transcript variants encoding the same protein have been identified. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Rab5, CAN, miR, OUT, POR
Papers on Rab23
Gene expression profiling of DMU-212-induced apoptosis and anti-angiogenesis in vascular endothelial cells.
Zhang et al., Zhengzhou, China. In Pharm Biol, Nov 2015
RESULTS AND CONCLUSION: DMU-212 was found to regulate a diverse range of genes, including cytokines (IL8, selectin E, MPZL2, EGR1, CCL20, ITGB8, CXCL1, VCAM1, KITLG, and AREG), transport proteins (TRPC4, SLC41A2, SLC17A5, and CREB5), metabolism (CYP1B1, CYP1A1, PDK4, CSNK1G1, MVK, TCEB3C, and CDKN3), enzymes (RAB23, SPHK1, CHSY3, PLAU, PLA2G4C, and MMP10), and genes involved in signal transduction (TMEM217, DUSP8, and SPRY4), chromosome organization (HIST1H2BH and GEM), cell migration and angiogenesis (ERRFI1, HBEGF, and NEDD9), and apoptosis (TNFSF15, TNFRSF9, CD274, BCL2L11, BIRC3, TNFAIP3, and TIFA), as well as other genes with unknown function (PGM5P2, SNORD1142, LOC151760, KRTAP5-2, C1orf110, SNORA14A, MIR31, C2CD4B, SCARNA4, C2orf66, SC4MOL, LOC644714, and LOC283392).
miR-367 promotes proliferation and stem-like traits in medulloblastoma cells.
Okamoto et al., São Paulo, Brazil. In Cancer Sci, Sep 2015
A concurrent downregulation of the miR-367 cancer-related targets RYR3, ITGAV and RAB23, was also detected in miR-367-overexpressing cells.
Prenatal findings in carpenter syndrome and a novel mutation in RAB23.
Toutain et al., Tours, France. In Am J Med Genet A, 2014
Carpenter syndrome is caused by mutations of the RAB23 gene.
Carpenter syndrome: a review for the craniofacial surgeon.
Wood-Smith et al., New York City, United States. In J Craniofac Surg, 2014
RESULTS: Mutations in RAB23 have been implicated in the pathogenesis of CS.
miR-200b as a prognostic factor targets multiple members of RAB family in glioma.
Jiang et al., Changsha, China. In Med Oncol, 2014
Members of RAB family, RAB21, RAB23, RAB18 and RAB3B were predicted to be novel targets of miR-200b.
miR-200b as a prognostic factor in breast cancer targets multiple members of RAB family.
Xie et al., Guangzhou, China. In J Transl Med, 2013
Members of RAB family, RAB21, RAB23, RAB18 and RAB3B were predicted to be the targets of miR-200b.
Gene expression signatures differentiate uterine endometrial stromal sarcoma from leiomyosarcoma.
Wang et al., Oslo, Norway. In Gynecol Oncol, 2013
Genes overexpressed in LMS included CDKN2A, FABP3, TAGLN, JPH2, GEM, NAV2 and RAB23.
A Novel Aberrant Splice Site Mutation in RAB23 Leads to an Eight Nucleotide Deletion in the mRNA and Is Responsible for Carpenter Syndrome in a Consanguineous Emirati Family.
Al-Gazali et al., United Arab Emirates. In Mol Syndromol, 2013
Carpenter syndrome is caused by mutations in the RAB23 gene that encodes a small GTPase of the Rab subfamily of proteins.
Array analysis for potential biomarker of gemcitabine identification in non-small cell lung cancer cell lines.
Shi et al., Harbin, China. In Int J Clin Exp Pathol, 2012
Genes whose expression increased dramatically in sensitive cell lines were mainly enriched in cell adhesion (NRP2, CXCR3, CDK5R1, IL32 and CDH2) and secretory granule (SLC11A1, GP5, CD36 and IGF1), while genes with significantly upregulated expression in resistant cell line were mainly clustered in methylation modification (HIST1H2BF, RAB23 and TP53) and oxidoreductase (TP53I3, CYP27B1 and SOD3).
Mutations in multidomain protein MEGF8 identify a Carpenter syndrome subtype associated with defective lateralization.
Wilkie et al., Oxford, United Kingdom. In Am J Hum Genet, 2012
Mutations of RAB23, encoding a small GTPase that regulates vesicular transport, are present in the majority of cases.
The small GTPases Rab9A and Rab23 function at distinct steps in autophagy during Group A Streptococcus infection.
Nakagawa et al., Tokyo, Japan. In Cell Microbiol, 2012
Rab9A and Rab23 GTPases play crucial roles in autophagy of Group A Streptococcus.
Rab23 negatively regulates Gli1 transcriptional factor in a Su(Fu)-dependent manner.
Xie et al., Indianapolis, United States. In Cell Signal, 2012
Rab23 directly associates with Su(Fu) and inhibits Gli1 function in a Su(Fu)-dependent manner.
Deregulation of Rab and Rab effector genes in bladder cancer.
Goud et al., Paris, France. In Plos One, 2011
Five of these deregulated genes (LEPRE1, MICAL2, RAB23, STXBP1, SYTL1) were specifically deregulated in FGFR3-non-mutated muscle-invasive tumors.
A genome-wide association study reveals evidence of association with sarcoidosis at 6p12.1.
GenPhenReSa Consortium et al., Kiel, Germany. In Eur Respir J, 2011
association of the 6p12.1 locus with sarcoidosis implicates this locus as a further susceptibility factor and RAB23 as a potential signalling component
Carpenter syndrome: extended RAB23 mutation spectrum and analysis of nonsense-mediated mRNA decay.
Wilkie et al., Oxford, United Kingdom. In Hum Mutat, 2011
Carpenter syndrome: extended RAB23 mutation spectrum and analysis of nonsense-mediated mRNA decay
Genetic basis of potential therapeutic strategies for craniosynostosis.
Jabs et al., New York City, United States. In Am J Med Genet A, 2010
The most common genetic mutations identified in syndromic craniosynostosis involve the fibroblast growth factor receptor (FGFR) family with other mutations occurring in genes for transcription factors TWIST, MSX2, and GLI3, and other proteins EFNB1, RAB23, RECQL4, and POR, presumed to be involved either upstream or downstream of the FGFR signaling pathway.
RAB23 mutation in a large family from Comoros Islands with Carpenter syndrome.
Cormier-Daire et al., Tours, France. In Am J Med Genet A, 2010
A RAB23 mutation (c.86dupA) present in the homozygote state in four relatives of Comorian origin with Carpenter syndrome, is reported.
Genetics of craniosynostosis: genes, syndromes, mutations and genotype-phenotype correlations.
Yeh et al., São Paulo, Brazil. In Front Oral Biol, 2007
Mutations in 7 genes are unequivocally associated with mendelian forms of syndromic craniosynostosis: FGFR1, FGFR2, FGFR3, TWIST1, EFNB1, MSX2 and RAB23.
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