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Collagen, type III, alpha 1

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?
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
Familial occurrence and heritable connective tissue disorders in cervical artery dissection.
CADISP-plus consortium et al., Aş Şanamayn, Syria. In Neurology, 25 Dec 2014
Two patients without a family history of CeAD had vascular Ehlers-Danlos syndrome with a mutation in COL3A1.
2-Methoxyestradiol inhibits bleomycin-induced systemic sclerosis through suppression of fibroblast activation.
Li et al., Shanghai, China. In J Dermatol Sci, 03 Dec 2014
In skin fibroblasts derived from SSc patients and healthy subjects treated with 2-ME (1, 5, or 25μM), we examined cell proliferation, expression of α-smooth muscle actin (SMA) and mRNA level of COL1A1, COL1A2, COL3A1, matrix metalloproteinase(MMP)-1 and tissue inhibitors of MMP (TIMP)-1.
Microarray-based detection and expression analysis of extracellular matrix proteins in drug‑resistant ovarian cancer cell lines.
Zabel et al., Poznań, Poland. In Oncol Rep, 30 Nov 2014
These genes were: ITGB1BP3, COL3A1, COL5A2, COL15A1, TGFBI, DCN, LUM, MATN2, POSTN and EGFL6.
High-level secretory expression and purification of unhydroxylated human collagen ɑ1(III) chain in Pichia pastoris GS115.
He et al., Xi'an, China. In Biotechnol Appl Biochem, Oct 2014
To obtain high-level secretory expression of single-chain full-length human collagen α1(III) chain (COL3A1) without the N and C telopeptides, the cDNA coding for the human COL3A1 gene was cloned into the secretory expression vector pPIC9K and integrated into Pichia pastoris GS115.
Vascular Ehlers-Danlos Syndrome in siblings with biallelic COL3A1 sequence variants and marked clinical variability in the extended family.
Byers et al., Tromsø, Norway. In Eur J Hum Genet, Oct 2014
UNLABELLED: Vascular Ehlers-Danlos Syndrome (vEDS), also known as EDS type IV, is considered to be an autosomal dominant disorder caused by sequence variants in COL3A1, which encodes the chains of type III procollagen.
Euphorbia hirta accelerates fibroblast proliferation and Smad-mediated collagen production in rat excision wound.
Veer et al., Tezpur, India. In Pharmacogn Mag, Aug 2014
Wound contraction, hydroxyproline content and the protein expression of COL3A1, bFGF, Smad-2,-3,-4 and -7 were measured.
Heritable thoracic aortic disorders.
Pyeritz, In Curr Opin Cardiol, Jan 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.
Dabus et al., Miami, United States. In Bmj Case Rep, Dec 2013
Ehlers-Danlos syndrome (EDS) type IV is a collagen vascular disease with an autosomal dominant inheritance caused by COL3A1 mutation.
Depletion of C3orf1/TIMMDC1 Inhibits Migration and Proliferation in 95D Lung Carcinoma Cells.
Xu et al., Zhenjiang, China. In Int J Mol Sci, Dec 2013
Furthermore, cell-cycle arrest genes such as CCNG2 and PTEN as well as genes involved in cell migration inhibition, such as TIMP3 and COL3A1, were upregulated after C3orf1 depletion in 95D cells.
Zhou et al., Houston, United States. In Eur J Inflamm, Sep 2013
The transcript levels of COL1A2, COL3A1, MIVIP1, MMP3, TIMP3 and CTGF genes of the fibroblasts were measured with quantitative RT-PCR.
A functional variant of the collagen type III alpha1 gene modify risk of sporadic intracranial aneurysms.
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.
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').
Genetic determinants of juvenile stroke.
Pezzini, Brescia, Italy. In Thromb Res, 2012
Furthermore, stroke is a well-known complication of several heritable connective tissue disorders, including Marfan's syndrome (FBN1 mutations) and Ehlers-Danlos syndrome type IV (COL3A1 mutations), which predispose to cervical artery dissection, the most frequent cause of cerebral ischemia at young age.
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.
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.
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.
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.
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.
Boutouyrie et al., Paris, France. In Lancet, 2010
33 patients were positive for mutation of collagen 3A1 (COL3A1).
Spontaneous arterial dissection: phenotype and molecular pathogenesis.
Gross-Weissmann et al., Heidelberg, Germany. In Cell Mol Life Sci, 2010
Genetic linkage analysis lead to the identification of mutations in different disease-causing genes involved in the biosynthesis of the extracellular matrix (FBN1, COL3A1), in transforming growth factor (TGF) beta signaling (FBN1, TGFBR1, TGFBR2) and in the SMC contractile system (ACTA2, MYH11).
Clinical and genetic features of Ehlers-Danlos syndrome type IV, the vascular type.
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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