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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Transforming growth factor, beta-induced, 68kDa

CSD, TGFBI, betaig-h3, BIGH3, keratoepithelin
This gene encodes an RGD-containing protein that binds to type I, II and IV collagens. The RGD motif is found in many extracellular matrix proteins modulating cell adhesion and serves as a ligand recognition sequence for several integrins. This protein plays a role in cell-collagen interactions and may be involved in endochondrial bone formation in cartilage. The protein is induced by transforming growth factor-beta and acts to inhibit cell adhesion. Mutations in this gene are associated with multiple types of corneal dystrophy. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, ACID, HAD, POLYMERASE, V1a
Papers using CSD antibodies
Proteome analysis of secreted proteins during osteoclast differentiation using two different methods: two-dimensional electrophoresis and isotope-coded affinity tags analysis with two-dimensional chromatography
Amri Ez-Zoubir et al., In BMC Molecular Biology, 2002
... Antibodies directed against ENO1, PEDF, BIGH3 and SPARC were supplied from Santa Cruz Biotechnology (Santa Cruz, CA), Chemicon ...
Papers on CSD
Autophagy in granular corneal dystrophy type 2.
Kim et al., Seoul, South Korea. In Exp Eye Res, Mar 2016
GCD2 is an autosomal dominant disorder caused by substitution of histidine for arginine at codon 124 (R124H) in the transforming growth factor β-induced gene (TGFBI) on chromosome 5q31.
Cortical spreading depolarization: Pathophysiology, implications, and future directions.
Liu et al., Los Angeles, United States. In J Clin Neurosci, Feb 2016
Cortical spreading depolarization (CSD) is a spreading loss of ion homeostasis, altered vascular response, change in synaptic architecture, and subsequent depression in electrical activity following an inciting neurological injury.
Pathophysiology of Corneal Dystrophies: From Cellular Genetic Alteration to Clinical Findings.
Lambiase et al., Milano, Italy. In J Cell Physiol, Feb 2016
Many corneal dystrophies have been genetically characterized and the specific gene mutations identified, such as for the epithelial-stromal TGFBI dystrophies.
The transformer genes in the fig wasp Ceratosolen solmsi provide new evidence for duplications independent of complementary sex determination.
Huang et al., Beijing, China. In Insect Mol Biol, Feb 2016
The honeybee Apis mellifera has two duplicates of tra, one of which (complementary sex determiner, csd) is the primary signal for complementary sex-determination (CSD), regulating the other duplicate (feminizer).
Mutational Spectrum of Korean Patients with Corneal Dystrophy.
Kim et al., Seoul, South Korea. In Clin Genet, Feb 2016
Epithelial-stromal TGFBI dystrophies, macular corneal dystrophy and Schnyder corneal dystrophy showed 100% mutation detection rates, while endothelial corneal dystrophies showed lower detection rates of 3%.
Interactive and Versatile Navigation of Structural Databases.
Stahl et al., Basel, Switzerland. In J Med Chem, Feb 2016
UNASSIGNED: We present CSD-CrossMiner, a novel tool for pharmacophore-based searches in crystal structure databases.
Pathogenesis and treatments of TGFBI corneal dystrophies.
Kim et al., Seoul, South Korea. In Prog Retin Eye Res, Jan 2016
Transforming growth factor beta-induced (TGFBI) corneal dystrophies are a group of inherited progressive corneal diseases.
Mouse chronic social stress increases blood and brain kynurenine pathway activity and fear behaviour: Both effects are reversed by inhibition of indoleamine 2,3-dioxygenase.
Pryce et al., Biberach an der Riß, Germany. In Brain Behav Immun, Jan 2016
The present mouse study investigated effects of psychosocial stress as chronic social defeat (CSD) versus control-handling (CON) on: Pavlovian tone-shock fear conditioning, activation of the kynurenine pathway, and efficacy of a specific inhibitor (IDOInh) of the tryptophan-kynurenine catabolising enzyme indoleamine 2,3-dioxygenase (IDO1), in reversing CSD effects on the kynurenine pathway and fear.
Facts and fictions about polymorphism.
Bernstein et al., Basel, Switzerland. In Chem Soc Rev, Jan 2016
We present new facts about polymorphism based on (i) crystallographic data from the Cambridge Structural Database (CSD, a database built over 50 years of community effort), (ii) 229 solid form screens conducted at Hoffmann-La Roche and Eli Lilly and Company over the course of 8+ and 15+ years respectively and (iii) a dataset of 446 polymorphic crystals with energies and properties computed with modern DFT-d methods.
Laminar Distribution of Phase-Amplitude Coupling of Spontaneous Current Sources and Sinks.
Shmuel et al., Montréal, Canada. In Front Neurosci, 2014
We then computed time-series of frequency-band- and lamina-specific current source density (CSD), and PACs of CSD for all possible pairs of the classical frequency bands in the range of 1-150 Hz.
Identification of Novel and Conserved miRNAs in Leaves of In vitro Grown Citrus reticulata "Lugan" Plantlets by Solexa Sequencing.
Lai et al., Fuzhou, China. In Front Plant Sci, 2014
After analyzing the expression level of their targets during the reservation of the ponkan in vitro plantlet, development-associated cre-ARF6 and stress-related cre-CSD modules exhibited negative correlation with miR167 and miR398, respectively, indicating an involvement of the miRNAs in the in vitro development of ponkan and function in the conservation of ponkan germplasm.
Spreading depression triggers headache by activating neuronal Panx1 channels.
Dalkara et al., Ankara, Turkey. In Science, 2013
Here, we describe a previously unknown signaling pathway between stressed neurons and trigeminal afferents during cortical spreading depression (CSD), the putative cause of migraine aura and headache.
In vitro amyloid aggregate forming ability of TGFBI mutants that cause corneal dystrophies.
Pang et al., Hong Kong, Hong Kong. In Invest Ophthalmol Vis Sci, 2012
our study confirmed the tight genotype-phenotype relationship of TGFBI gene-linked corneal dystrophies.
The point mutation and polymorphism in keratoconus candidate gene TGFBI in Chinese population.
Ding et al., Linhai, China. In Gene, 2012
The candidate keratoconus gene TGFB1 showed genetic variation and mutation in the keratoconus population. The gene might play a role in the development of keratoconus in the Chinese population.
Lysophosphatidic acid activates TGFBIp expression in human corneal fibroblasts through a TGF-β1-dependent pathway.
Kim et al., Seoul, South Korea. In Cell Signal, 2012
Lysophosphatidic acid induces TGFBI expression by stimulating secretion of TGF-beta 1.
Transforming growth factor beta-induced (TGFBI) is an anti-adhesive protein regulating the invasive growth of melanoma cells.
Hölttä et al., Helsinki, Finland. In Am J Pathol, 2012
These data imply an important role for TGFBI in the extracelular matrix deposition and invasive growth of melanoma cells, rendering it a potential target for therapeutic interventions.
Extremely varied phenotypes in granular corneal dystrophy type 2 heterozygotes.
Kim et al., Seoul, South Korea. In Mol Vis, 2011
There is drastic phenotypic variability in patients with the heterozygous R124H mutation in the TGFBI gene that causes granular corneal dystrophy type 2 in Korean patients.
Effects of tonabersat on migraine with aura: a randomised, double-blind, placebo-controlled crossover study.
Olesen et al., Glostrup, Denmark. In Lancet Neurol, 2009
BACKGROUND: Migraine with aura is thought likely to be caused by cortical spreading depression (CSD).
The extracellular matrix protein TGFBI induces microtubule stabilization and sensitizes ovarian cancers to paclitaxel.
Brenton et al., Cambridge, United Kingdom. In Cancer Cell, 2007
Loss of the extracellular matrix protein TGFBI (transforming growth factor beta induced) is sufficient to induce specific resistance to paclitaxel and mitotic spindle abnormalities in ovarian cancer cells.
MC1R germline variants confer risk for BRAF-mutant melanoma.
Bastian et al., Bethesda, United States. In Science, 2006
The majority of melanomas that occur on skin with little evidence of chronic sun-induced damage (non-CSD melanoma) have mutations in the BRAF oncogene, whereas in melanomas on skin with marked CSD (CSD melanoma) these mutations are less frequent.
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