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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 30 Mar 2015.

Collagen, type III, alpha 1

COL3A1
This gene encodes the pro-alpha1 chains of type III collagen, a fibrillar collagen that is found in extensible connective tissues such as skin, lung, uterus, intestine and the vascular system, frequently in association with type I collagen. Mutations in this gene are associated with Ehlers-Danlos syndrome types IV, and with aortic and arterial aneurysms. Two transcripts, resulting from the use of alternate polyadenylation signals, have been identified for this gene. [provided by R. Dalgleish, Feb 2008] (from NCBI)
Top mentioned proteins: COL1A1, HAD, CAN, POLYMERASE, ACID
Papers using COL3A1 antibodies
Receptor-independent actions of PPAR thiazolidinedione agonists: is mitochondrial function the key?
Supplier
Bourke Jane E et al., In Respiratory Research, 2004
... Quantitect primers for the human genes COL1A1, COL3A1 and 18s rRNA were from Qiagen (Hilden, Germany) and the ...
Papers on COL3A1
Ehlers-Danlos syndrome type IV is associated with a novel G984R COL3A1 mutation.
New
Yang et al., Changsha, China. In Mol Med Report, 13 Apr 2015
Mutations in COL3A1 have been identified to underlie this disease; however, to the best of our knowledge, no COL3A1 mutations have been reported in Ehlers‑Danlos syndrome type IV patients with an ascending aortic aneurysm.
The type of variants at the COL3A1 gene associates with the phenotype and severity of vascular Ehlers-Danlos syndrome.
New
Jeunemaitre et al., Paris, France. In Eur J Hum Genet, 11 Apr 2015
UNASSIGNED: Vascular Ehlers-Danlos syndrome (vEDS) is a rare and severe autosomal dominant disorder caused by variants at the COL3A1 gene.
Dexamethasone Controlled Release on TGF-β1 Treated Vocal Fold Fibroblasts.
New
Sivasankar et al., West Lafayette, United States. In Ann Otol Rhinol Laryngol, 09 Mar 2015
RESULTS: COL3A1 and COL1A2 were significantly down-regulated after exposure to ester-terminated low molecular weight PLGA microparticles loaded with dexamethasone.
Gene panel sequencing in heritable thoracic aortic disorders and related entities ¿ results of comprehensive testing in a cohort of 264 patients.
New
De Backer et al., In Orphanet J Rare Dis, 03 Mar 2015
So far, no data on mutation detection rate with this technique have been reported.MethodsWe performed Next Generation Sequencing (NGS) based screening of the seven currently most prevalent H-TAD-associated genes (FBN1, TGFBR1/2, TGFB2, SMAD3, ACTA2 and COL3A1) on 264 samples from unrelated probands referred for H-TAD and related entities.
Myofibroblast Expression in Skin Wounds Is Enhanced by Collagen III Suppression.
New
Shier et al., Riyadh, Saudi Arabia. In Biomed Res Int, Dec 2014
One exception is seen in patients and animal models of Ehlers-Danlos syndrome type IV in which the COL3A1 gene mutation results in reduced collagen III but with concurrent increased myofibroblast expression.
Transcriptome comparisons identify new cell markers for theca interna and granulosa cells from small and large antral ovarian follicles.
New
Rodgers et al., Adelaide, Australia. In Plos One, Dec 2014
Many genes up regulated in theca interna were common to both sizes of follicles (MGP, DCN, ASPN, ALDH1A1, COL1A2, FN1, COL3A1, OGN, APOD, COL5A2, IGF2, NID1, LHFP, ACTA2, DUSP12, ACTG2, SPARCL1, FILIP1L, EGFLAM, ADAMDEC1, HPGD, COL12A1, FBLN5, RAMP2, COL15A1, PLK2, COL6A3, LOXL1, RARRES1, FLI1, LAMA2).
Identification of suitable reference genes for gene expression studies in tendons from patients with rotator cuff tear.
New
Cohen et al., São Paulo, Brazil. In Plos One, Dec 2014
To identify the optimal combination of reference genes, we evaluated the expression of COL1A1 and COL3A1, and no obvious differences were observed when using 2, 3 or 4 reference genes for most of the analyses.
miR-29a/b Enhances Cell Migration and Invasion in Nasopharyngeal Carcinoma Progression by Regulating SPARC and COL3A1 Gene Expression.
New
Zhang et al., Guangzhou, China. In Plos One, Dec 2014
Furthermore, we demonstrated that miR-29a/b might be responsible for increasing S18 cell migration and invasion, and only COL3A1 was identified as a direct target of miR-29b despite the fact that both SPARC and COL3A1 were inhibited by miR-29a/b over-expression.
Genetic epidemiology of pelvic organ prolapse: a systematic review.
Review
New
Wu et al., Nashville, United States. In Am J Obstet Gynecol, Oct 2014
The metaanalysis suggests that collagen type 3 alpha 1 (COL3A1) rs1800255 genotype AA is associated with pelvic organ prolapse (odds ratio, 4.79; 95% confidence interval, 1.91-11.98;
Vascular type Ehlers-Danlos Syndrome with fatal spontaneous rupture of a right common iliac artery dissection: case report and review of literature.
Review
New
Cain et al., Louisville, United States. In J Radiol Case Rep, Feb 2014
Vascular Ehlers-Danlos Syndrome (previously Ehlers-Danlos IV) is a rare autosomal dominant collagen vascular disorder caused by a 2q31 COL3A1 gene mutation encoding pro-alpha1 chain of type III collagen (in contrast to classic Ehlers-Danlos, caused by a COL5A1 mutation).
Heritable thoracic aortic disorders.
Review
Pyeritz, In Curr Opin Cardiol, 2014
RECENT FINDINGS: A classification scheme based on the gene is emerging, those that affect primarily the extracellular matrix (e.g., FBN1, COL3A1), TGF-β signaling (e.g., TGFBR1, TGFB2), or vascular smooth muscle cell contractility (e.g., ACTA2, MYH11).
Endovascular repair of direct carotid-cavernous fistula in Ehlers-Danlos type IV.
Review
Dabus et al., Miami, United States. In Bmj Case Rep, 2013
Ehlers-Danlos syndrome (EDS) type IV is a collagen vascular disease with an autosomal dominant inheritance caused by COL3A1 mutation.
A functional variant of the collagen type III alpha1 gene modify risk of sporadic intracranial aneurysms.
GeneRIF
Hui et al., Beijing, China. In Hum Genet, 2012
study found that allele A of SNP rs1800255 conferred a 1.71-fold increased risk for intracranial aneurysms (IAs) and results in an amino acid change of Ala698Thr, which led to a lower thermal stability of the peptide; results support the view that the functional variant of COL3A1 is genetic risk factors for IAs in the Chinese population
Defining requirements for collagenase cleavage in collagen type III using a bacterial collagen system.
GeneRIF
Brodsky et al., United States. In J Biol Chem, 2012
The minimum type III sequence necessary for cleavage by the MMP1 and MMP13 was 5 GXY triplets, including 4 residues before and 11 residues after the cleavage site (P4-P11').
Changes in serum histologic surrogate markers and procollagen III N-terminal peptide as independent predictors of HBeAg loss in patients with chronic hepatitis B during entecavir therapy.
GeneRIF
Cheong et al., Suwŏn, South Korea. In Clin Biochem, 2012
procollagen III N-terminal peptide has a role in HBeAg loss in patients with chronic hepatitis B during entecavir therapy
Vascular Ehlers-Danlos syndrome: pathophysiology, diagnosis, and prevention and treatment of its complications.
Review
Frishman et al., Mount Vernon, United States. In Cardiol Rev, 2012
VEDS is inherited as an autosomal dominant trait that is caused by mutations in the COL3A1 gene.
Loss of Col3a1, the gene for Ehlers-Danlos syndrome type IV, results in neocortical dyslamination.
GeneRIF
Piao et al., Boston, United States. In Plos One, 2011
a possible common pathological pathway linking connective tissue diseases and brain malformations
Disease-associated mutations prevent GPR56-collagen III interaction.
GeneRIF
Piao et al., Boston, United States. In Plos One, 2011
Disease-associated mutations prevent GPR56-collagen III interaction.
Effect of celiprolol on prevention of cardiovascular events in vascular Ehlers-Danlos syndrome: a prospective randomised, open, blinded-endpoints trial.
Impact
Boutouyrie et al., Paris, France. In Lancet, 2010
33 patients were positive for mutation of collagen 3A1 (COL3A1).
Clinical and genetic features of Ehlers-Danlos syndrome type IV, the vascular type.
Impact
Byers et al., Seattle, United States. In N Engl J Med, 2000
BACKGROUND: Ehlers-Danlos syndrome type IV, the vascular type, results from mutations in the gene for type III procollagen (COL3A1).
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