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Data suggest that, compared with obese white women, obese black women exhibit higher expression of HIF1A (hypoxia inducible factor 1 alpha (show HIF1A Antibodies)), COL5A1 (show COL5A1 Antibodies) (collagen Valpha1), and COL6A1 (collagen VIalpha1) in gluteal but not abdominal subcutaneous adipose tissue depots; up-regulation of expression of these proteins correlates with reduced insulin (show INS Antibodies) sensitivity in black women only.
COL6A1 may have a role in progression and outcome of clear cell renal cell carcinoma (show MOK Antibodies)
worsening of the functional disability appeared typically after the age of 40 in 47% of our patients with Bethlem myopathy, and was frequently associated with COL6A1 exon 14 skipping
The second main finding of this study was that COL6A1 rs35796750 did not associate with the risk of anterior cruciate ligament injury in the self-reported Caucasian South African cohort.
Data indicate that collagen-VI-alpha-1 (COL6A1) is expressed in all grades of glioma.
Parental mosaicism was confirmed in the four families through quantitative analysis of the ratio of mutant versus wild-type allele (COL6A1, COL6A2 (show COL6A2 Antibodies), and COL6A3 (show COL6a3 Antibodies)) in genomic DNA from various tissues; consistent with somatic mosaicism, parental samples had lower ratios of mutant versus wild-type allele compared with the fully heterozygote offspring.
In UCDM, 1 mutation was indentified in COL6A1 in Chinese patients.
These results suggest that these SNPs of BMP-2 (show BMP2 Antibodies) and COL6A1 may not directly influence the expression of OPLL.
Absence of ANXA2 (show ANXA2 Antibodies) leads to retention of COL6 in a late-Golgi, VAMP2 (show VAMP2 Antibodies)-positive compartment.
Mutations in each of the three collagen VI genes, COL6A1, COL6A2 (show COL6A2 Antibodies) and COL6A3 (show COL6a3 Antibodies), cause four types of muscle disorders: Ullrich congenital muscular dystrophy, Bethlem myopathy, limb-girdle muscular dystrophy, and autosomal recessive myosclerosis. (Review)
This study demonstrates that Col6a1-Cre driver mice are as useful as Twist2 (show TWIST2 Antibodies)-Cre driver mice for functional analyses of GALT (show GALT Antibodies)-resident mesenchymal cells, including MCi (show MCIN Antibodies) cells.
Confocal laser scanning microscopy co-localised perlecan (show HSPG2 Antibodies) with type VI collagen as pericellular components of intervertebral disc (IVD (show IVD Antibodies)) cells and translamellar cross-bridges in ovine and murine IVDs.
this paper shows deregulation of the circadian rhythmic process in Col6a1-/- mice
Results show that a lack of collagen VI in Col6a1 -/- mice prevents macrophage recruitment and phenotypic transition after sciatic nerve crush, which in turn inhibits peripheral nervous system regeneration
Col6a1 was not required for TRPV4 (show TRPV4 Antibodies)-mediated Ca signaling. Knockout of Col6a1 altered the mechanical properties of the pericellular matrix, which increased the extent of cell swelling and osmotically induced TRPV4 (show TRPV4 Antibodies) signaling in an age-dependent manner.
Detected is a decreased tensile strength of the skin and an altered collagen fibril and basement membrane architecture in Col6a1 null mice, the latter being features that are also found in collagen VI myopathy patients.
Lack of collagen VI in Col6a1(-/-) mice causes impaired muscle regeneration and reduced satellite cell self-renewal capability after injury.
The expression of Col6a1 in 10T1/2 was also significantly higher than that in other feeder cells. It promoted the colony formation of epithelial cells in vitro effectively.
Physical training exacerbated the dystrophic phenotype of Col6a1-/- mice, where autophagy flux is compromised.
the accumulation of abnormal mitochondria and sarcoplasmic reticulum is caused by a defect of autophagy and that restoration of a proper autophagic flux in Col6a1-/- muscles ameliorates these alterations.
The collagens are a superfamily of proteins that play a role in maintaining the integrity of various tissues. Collagens are extracellular matrix proteins and have a triple-helical domain as their common structural element. Collagen VI is a major structural component of microfibrils. The basic structural unit of collagen VI is a heterotrimer of the alpha1(VI), alpha2(VI), and alpha3(VI) chains. The alpha2(VI) and alpha3(VI) chains are encoded by the COL6A2 and COL6A3 genes, respectively. The protein encoded by this gene is the alpha 1 subunit of type VI collagen (alpha1(VI) chain). Mutations in the genes that code for the collagen VI subunits result in the autosomal dominant disorder, Bethlem myopathy.
collagen, type VI, alpha 1
, type IV collagen alpha 1 subunit
, alpha-1 type VI collagen
, collagen alpha-1(VI) chain
, alpha 1 (VI) chain (61 AA)
, collagen VI, alpha-1 polypeptide
, collagen type VI alpha 1
, procollagen, type VI, alpha 1
, collagen VI-alpha1 protein
, type VI collagen alpha 3 chain