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Cellular retinoic acid binding protein 1

CRABP, CRABP I, CRABP1, cellular retinoic acid binding protein I
This gene encodes a specific binding protein for a vitamin A family member and is thought to play an important role in retinoic acid-mediated differentiation and proliferation processes. It is structurally similar to the cellular retinol-binding proteins, but binds only retinoic acid at specific sites within the nucleus, which may contribute to vitamin A-directed differentiation in epithelial tissue. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: ACID, CRBP, CRABP-II, RAR, CAN
Papers on CRABP
Ectopic cross-talk between thyroid and retinoic acid signaling: A possible etiology for spinal neural tube defects.
Zhang et al., Beijing, China. In Gene, Jan 2016
The promoters of the RA signaling genes CRABP1 and RARB were ectopically occupied by increased RXRG and RXRB but displayed decreased levels of inhibitory histone modifications, suggesting that elevated TH signaling abnormally stimulates RA signaling genes.
miR-93/miR-106b/miR-375-CIC-CRABP1: a novel regulatory axis in prostate cancer progression.
Lee et al., South Korea. In Oncotarget, Oct 2015
We found that knock-down of CIC derepresses expression of ETV5 and CRABP1 in LNCaP and PC-3 cells, respectively, thereby promoting cell proliferation and invasion.
Intracellular transport of fat-soluble vitamins A and E.
Arai et al., Tokyo, Japan. In Traffic, 2015
Vitamin A and its derivatives, collectively called retinoids, are solubilized by intracellular retinoid-binding proteins such as cellular retinol-binding protein (CRBP), cellular retinoic acid-binding protein (CRABP) and cellular retinal-binding protein (CRALBP).
Nuclear maspin expression correlates with the CpG island methylator phenotype and tumor aggressiveness in colorectal cancer.
Kang et al., Seoul, South Korea. In Int J Clin Exp Pathol, 2014
CIMP status was also determined by methylation-specific quantitative PCR method (MethyLight) using eight CIMP markers (MLH1, NEUROG1, CRABP1, CACNA1G, CDKN2A (p16), IGF2, SOCS1, and RUNX3) in 216 MSI-H CRCs.
Expression of retinoic acid-binding proteins and retinoic acid receptors in sebaceous cell carcinoma of the eyelids.
Yeh et al., Taiwan. In Bmc Ophthalmol, 2014
Immunohistochemical staining for β-catenin, cellular retinoic acid binding protein 1 (CRABP1), cellular retinoic acid binding protein 2 (CRABP2), fatty acid-binding protein 5 (FABP5), retinoic acid receptors (RAR-α, -β, -γ), and retinoid X receptors (RXR-α, -β, -γ) was performed on tissue samples obtained from tumor excision.
CRABP1 is associated with a poor prognosis in breast cancer: adding to the complexity of breast cancer cell response to retinoic acid.
Godbout et al., Edmonton, Canada. In Mol Cancer, 2014
The expression and subcellular distribution of two RA-binding proteins, FABP5 and CRABP2, has already been shown to play critical roles in breast cancer cell response to RA. CRABP1, a third member of the RA-binding protein family, has not previously been investigated as a possible mediator of RA action in breast cancer.
Chromatin remodeling and epigenetic regulation of the CrabpI gene in adipocyte differentiation.
Wei, Minneapolis, United States. In Biochim Biophys Acta, 2012
In cytoplasm, RA binds specifically to cellular retinoic acid binding proteins I (CRABPI), and II.
Expression of CRABP1, GRP, and RERG mRNA in clinically non-functioning and functioning pituitary adenomas.
Giorgi et al., São Paulo, Brazil. In J Endocrinol Invest, 2011
Results describe the mRNA expression of CRABP1, RERG, and GRP in pituitary adenomas.
CRABP1-reduced expression is associated with poorer prognosis in serous and clear cell ovarian adenocarcinoma.
Kimura et al., Sakai, Japan. In J Cancer Res Clin Oncol, 2011
reduced expression of CRABP1 has a potential as a prognostic marker for serous adenocarcinoma which is the most frequent histological ovarian tumor type and also for clear cell carcinoma that often exhibits chemo-resistance.
Prognostic significance of CDKN2A (p16) promoter methylation and loss of expression in 902 colorectal cancers: Cohort study and literature review.
Ogino et al., Boston, United States. In Int J Cancer, 2011
We analyzed for LINE-1 hypomethylation and hypermethylation at 7 CIMP-specific CpG islands (CACNA1G, CRABP1, IGF2, MLH1, NEUROG1, RUNX3 and SOCS1); microsatellite instability (MSI); KRAS, BRAF and PIK3CA mutations; and expression of TP53 (p53), CTNNB1 (β-catenin), CDKN1A (p21), CDKN1B (p27), CCND1 (cyclin D1), FASN (fatty acid synthase) and PTGS2 (cyclooxygenase-2).
Retinoid pathway and cancer therapeutics.
Wan et al., Kansas City, United States. In Adv Drug Deliv Rev, 2010
Retinoids exert their effects through a variety of binding proteins including cellular retinol-binding protein (CRBP), retinol-binding proteins (RBP), cellular retinoic acid-binding protein (CRABP), and nuclear receptors i.e. retinoic acid receptor (RAR) and retinoid x receptor (RXR).
Retinoid pathway and congenital diaphragmatic hernia: hypothesis from the analysis of chromosomal abnormalities.
Tchirkov et al., Clermont-Ferrand, France. In Fetal Diagn Ther, 2009
We propose other candidates such as STRA6, LRAT, CRBP1, CRBP2 and CRABP1 are directly implicated in retinoic acid metabolism.
LIF removal increases CRABPI and CRABPII transcripts in embryonic stem cells cultured in retinol or 4-oxoretinol.
Gudas et al., Austin, United States. In Mol Cell Endocrinol, 2008
Increases in CRABPI and II transcripts in the absence of leukemia inhibitory factor may regulate aspects of embryonic stem cell differentiation in response to retinol.
Upregulation of CRABP1 in human neuroblastoma cells overproducing the Alzheimer-typical Abeta42 reduces their differentiation potential.
Hartmann et al., Heidelberg, Germany. In Bmc Med, 2007
The authors identified several dysregulated genes and proteins, but only the cellular retinoic acid binding protein 1 (CRABP1) was up-regulated exclusively in cells expressing an increased Abeta42/Abeta40 ratio.
RARalpha-PLZF overcomes PLZF-mediated repression of CRABPI, contributing to retinoid resistance in t(11;17) acute promyelocytic leukemia.
Grimwade et al., London, United Kingdom. In Proc Natl Acad Sci U S A, 2007
supports an active role for PLZF and RARalpha-PLZF in leukemogenesis, identifies up-regulation of CRABPI
Opposing effects of retinoic acid on cell growth result from alternate activation of two different nuclear receptors.
Noy et al., Ithaca, United States. In Cell, 2007
Partitioning of RA between the two receptors is regulated by the intracellular lipid binding proteins CRABP-II and FABP5.
Meta-analysis and meta-review of thyroid cancer gene expression profiling studies identifies important diagnostic biomarkers.
Wiseman et al., Vancouver, Canada. In J Clin Oncol, 2006
A review of the top 12 candidates revealed well known thyroid cancer markers such as MET, TFF3, SERPINA1, TIMP1, FN1, and TPO as well as relatively novel or uncharacterized genes such as TGFA, QPCT, CRABP1, FCGBP, EPS8 and PROS1.
Pathogenesis of HIV-1-protease inhibitor-associated peripheral lipodystrophy, hyperlipidaemia, and insulin resistance.
Cooper et al., Sydney, Australia. In Lancet, 1998
The catalytic region of HIV-1 protease, to which protease inhibitors bind, has approximately 60% homology to regions within two proteins that regulate lipid metabolism: cytoplasmic retinoic-acid binding protein type 1 (CRABP-1) and low density lipoprotein-receptor-related protein (LRP).
The retinoid ligand 4-oxo-retinoic acid is a highly active modulator of positional specification.
Durston et al., Utrecht, Netherlands. In Nature, 1993
The pleiotropic effects of retinoids may be explained by the existence of complex signal transduction pathways involving diverse nuclear receptors of the retinoic acid receptor (RAR) and retinoid X receptor (RXR) families, and at least two types of cellular retinoic acid binding proteins (CRABP-I and -II).
Spatial distribution of cellular protein binding to retinoic acid in the chick limb bud.
Chytil et al., London, United Kingdom. In Nature, 1988
It has been proposed that retinoic acid acts by binding to a cellular retinoic acid-binding protein (CRABP) and then entering the nucleus to alter the pattern of gene activity.
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