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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
Aryl hydrocarbon receptor-driven signals inhibit collagen synthesis in the gut.
New
Monteleone et al., Roma, Italy. In Eur J Immunol, Feb 2016
In CD fibroblasts, TGF-β1 and TNF-α increased Col1A1, Col3A1 and α-SMA transcripts and collagen secretion and this effect was reduced by Ficz and upregulated by CH22319.
Osteogenic potential of human adipose-tissue derived mesenchymal stromal cells cultured on 3D-printed porous structured titanium.
New
van Wijnen et al., Rochester, United States. In Gene, Feb 2016
Compared to standard tissue culture plastic, AMSCs grown in the porous titanium microenvironment showed differences in temporal expression for genes involved in cell cycle progression (CCNB2, HIST2H4), extracellular matrix production (COL1A1, COL3A1), mesenchymal lineage identity (ACTA2, CD248, CD44), osteoblastic transcription factors (DLX3, DLX5, ID3) and epigenetic regulators (EZH1, EZH2).
Epithelial but not stromal expression of collagen alpha-1(III) is a diagnostic and prognostic indicator of colorectal carcinoma.
New
Liu et al., Shanghai, China. In Oncotarget, Feb 2016
Collagen alpha-1(III) (COL3A1) gene, encoding an extracellular matrix protein, is upregulated in human cancers.
Dioscin alleviates BDL- and DMN-induced hepatic fibrosis via Sirt1/Nrf2-mediated inhibition of p38 MAPK pathway.
New
Peng et al., Dalian, China. In Toxicol Appl Pharmacol, Jan 2016
Furthermore, dioscin markedly up-regulated the levels of sirtuin 1 (Sirt1), HO-1, GST, GCLC and GCLM via increasing the nuclear translocation of nuclear erythroid factor 2-related factor 2 (Nrf2), which in turn inhibited mitogen-activated protein kinase 14 (p38 MAPK) phosphorylation and reduced the levels of COL1A1, COL3A1, α-SMA and fibronectin.
RNA sequencing identifies crucial genes in papillary thyroid carcinoma (PTC) progression.
New
Sun et al., Qingdao, China. In Exp Mol Pathol, Jan 2016
Hub nodes in the PPI network were RRM2 and a set of collagens (COL1A1, COL3A1 and COL5A1), which were also remarkable in module 3 and module 5, respectively.
Autologous leukocyte-reduced platelet-rich plasma therapy for Achilles tendinopathy induced by collagenase in a rabbit model.
New
Carmona et al., Manizales, Colombia. In Sci Rep, Dec 2015
We compared, at 4 and 12 weeks (w), the LR-PRP and placebo (PBS) effects on ultrasonography, histology and relative gene expression of collagen types I (COL1A1) and III (COL3A1) and vascular endothelial growth factor (VEGF) in 24 rabbits with TAT induced by collagenase.
Genetics of hereditary large vessel diseases.
Review
New
Morisaki et al., Ōsaka, Japan. In J Hum Genet, Nov 2015
Genes identified for these diseases include FBN1, TGFBR1, TGFBR2, SMAD3, TGFB2, TGFB3, SKI, EFEMP2, COL3A1, FLNA, ACTA2, MYH11, MYLK and SLC2A10, as well as others.
Systematic review and metaanalysis of genetic association studies of urinary symptoms and prolapse in women.
Review
New
Khullar et al., London, United Kingdom. In Am J Obstet Gynecol, Feb 2015
Other metaanalyses, including those for polymorphisms of COL3A1,LAMC1,MMP1,MMP3, and MMP9 did not show significant effects.
Aortic Remodelling Is Improved by 2,3,5,4'-Tetrahydroxystilbene-2-O-β-D-glucoside Involving the Smad3 Pathway in Spontaneously Hypertensive Rats.
Xu et al., Shanghai, China. In Evid Based Complement Alternat Med, 2014
Orally administering THSG to spontaneously hypertensive rats (SHRs) aged 12 weeks for 14 weeks significantly inhibited intima-media thickness in the lower parts of the aortic arch, increased the vascular diastolic rate in response to acetylcholine, and reduced remodelling-related mRNA expression, such as that of ACTA2, CCL3, COL1A2, COL3A1, TIMP1 WISP2, IGFBP1, ECE1, KLF5, MYL1 BMP4, FN1, and PAI-1.
Ehlers-Danlos Syndrome Type IV with Bilateral Pneumothorax.
Nakano et al., Japan. In Intern Med, 2014
Ehlers-Danlos syndrome (EDS) was suspected due to the combination of colon perforation and pneumothorax, and EDS type IV was confirmed after a genetic study identified a c.1511g>a mutation in the COL3A1 gene.
Genetic epidemiology of pelvic organ prolapse: a systematic review.
Review
Wu et al., Nashville, United States. In Am J Obstet Gynecol, 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
Cain et al., Louisville, United States. In J Radiol Case Rep, 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).
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
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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