Collagen Type VI
Collagen
Extracellular Matrix Proteins
Collagen Type I
Immunoblotting
Collagen Type III
Collagen Type IV
Collagen Type II
Collagen Type V
Fibrillar Collagens
Bacterial Secretion Systems
Mucopolysaccharidosis VI
Collagen Type XI
Extracellular Matrix
Receptors, Collagen
N-Acetylgalactosamine-4-Sulfatase
Pepsin A
Fibroblasts
Glycogen Storage Disease Type VI
Cartilage
Collagen Type XVIII
Procollagen
Fibronectins
Cells, Cultured
Collagen Type X
Basement Membrane
Collagen Type XII
Decorin
Interstitial collagens I, III, and VI sequester and modulate the multifunctional cytokine oncostatin M. (1/145)
The binding of certain growth factors and cytokines to components of the extracellular matrix can regulate their local availability and modulate their biological activities. We show that oncostatin M (OSM), a profibrogenic cytokine and modulator of cancer cell proliferation, specifically binds to collagen types I, III, IV, and VI, immobilized on polystyrene or nitrocellulose. Single collagen chains inhibit these interactions in a dose-dependent manner. Cross-inhibition experiments of collagen-derived peptides point to a limited set of OSM-binding collagenous consensus sequences. Furthermore, this interaction is found for OSM but not for other interleukin-6 type cytokines. OSM binding to collagens is saturable, with dissociation constants around 10(-8) m and estimated molar ratios of 1-3 molecules of OSM bound to one molecule of triple helical collagen. Furthermore, collagen-bound OSM is biologically active and able to inhibit proliferation of A375 melanoma cells. We conclude that abundant interstitial collagens dictate the spatial pattern of bioavailable OSM. This interaction could be exploited for devising collagenous peptide-antagonists that modulate OSM bioactivity in tumor growth and fibrotic disorders like rheumatoid arthritis and hepatic fibrosis. (+info)Flexibility and packing in proteins. (2/145)
Structural flexibility is an essential attribute, without which few proteins could carry out their biological functions. Much information about protein flexibility has come from x-ray crystallography, in the form of atomic mean-square displacements (AMSDs) or B factors. Profiles showing the AMSD variation along the polypeptide chain are usually interpreted in dynamical terms but are ultimately governed by the local features of a highly complex energy landscape. Here, we bypass this complexity by showing that the AMSD profile is essentially determined by spatial variations in local packing density. On the basis of elementary statistical mechanics and generic features of atomic distributions in proteins, we predict a direct inverse proportionality between the AMSD and the contact density, i.e., the number of noncovalent neighbor atoms within a local region of approximately 1.5 nm(3) volume. Testing this local density model against a set of high-quality crystal structures of 38 nonhomologous proteins, we find that it accurately and consistently reproduces the prominent peaks in the AMSD profile and even captures minor features, such as the periodic AMSD variation within alpha helices. The predicted rigidifying effect of crystal contacts also agrees with experimental data. With regard to accuracy and computational efficiency, the model is clearly superior to its predecessors. The quantitative link between flexibility and packing density found here implies that AMSDs provide little independent information beyond that contained in the mean atomic coordinates. (+info)Differential gene expression in human abdominal aorta: aneurysmal versus occlusive disease. (3/145)
OBJECTIVE: Inflammation and atherosclerosis are present in both abdominal aortic aneurysm (AAA) and arterial occlusive disease (AOD). Changes in gene expression that underlie the development of AAA versus AOD are poorly defined. This study evaluated differences in gene expression in AAA, AOD, and control aortic tissue with human gene array technology. METHODS: RNA was isolated from human aortic specimens (seven AAA, five AOD, and five control), and complementary DNA (cDNA) probes were generated. The cDNA probes were hybridized to a human cell interaction array of 265 genes and quantitated with phosphorimaging. The data were corrected for background and were standardized to housekeeping genes. Statistical differences in individual gene expression were determined with the Kruskal-Wallis test. RESULTS: Of 265 genes studied, 11 showed statistically different expression in diseased aorta as compared with control. The following three genes were downregulated in AAA: collagen VI alpha1 (P <.037), glycoprotein IIIA (P <.006), and alpha2-macroglobulin (P <.020). The following two genes were upregulated in AOD: laminin alpha4 (P <.034) and insulin-like growth factor 2 receptor (P <.049). The following three genes were upregulated in both AAA and AOD: matrix metalloproteinase-9 (MMP-9; P <.005), intercellular adhesion molecule-1 (P <.012), and tumor necrosis factor--beta receptor (P <.022). The following three genes were downregulated in both AAA and AOD: integrin alpha5 (P <.012), ephrin A5 (P <.037), and rho/rac guanine nucleotide exchange factor (P <.028). Of 16 MMPs evaluated, only MMP-9 was significantly (P <.005) upregulated in both AAA and AOD. Evaluation results of four tissue inhibitors of metalloproteinases showed no significant difference in expression for all tissue types, although tissue inhibitor of metalloproteinase-1 trended toward upregulation in AAA (P =.053). Eight of the fifteen most highly expressed genes in all the groups were extracellular matrix or secreted proteins. Of these, only collagen VI alpha1 (P <.037) showed a significant change, although biglycan trended toward downregulation in AAA (P =.076). CONCLUSION: This study used cDNA array technology in the comparison of human control and pathologic aortic tissue. Six genes had similar differential expression in both AAA and AOD as compared with control. Even more interesting were differences between AAA and AOD in the expression of five genes. These data suggest a similarity in genetic expression for both AAA and AOD, with altered expression of several genes playing a role in disease differentiation. (+info)Antibody response against perlecan and collagen types IV and VI in chronic renal allograft rejection in the rat. (4/145)
Chronic rejection is the leading cause of late renal transplant failure. Various structural lesions are observed in grafts undergoing chronic rejection including glomerular basement membrane (GBM) duplications. The well-established Fisher (F344) to Lewis (LEW) rat renal transplant model for chronic rejection was used to assess the presence and role of the humoral immune response against graft antigens during chronic rejection. LEW recipients of F344 allografts develop transplant glomerulopathy and produce IgG1 antibodies directed against F344 GBM preparations that are detectable 3 weeks after transplantation. Glomerular IgG1 deposition was observed that in vitro co-localized with a rabbit anti-rat GBM antiserum in rejecting F344 grafts; elution experiments of isolated glomeruli yielded IgG1 antibodies reactive in vitro with F344 GBM, but not LEW GBM. Prevention of acute rejection by transient treatment of the recipients with cyclosporin A completely abrogated the production of anti-GBM antibodies. Using proteomic techniques we identified the antigens recognized by the LEW posttransplant sera as being the heparan sulfate proteoglycan perlecan and the alpha1 chain of collagen type VI in association with the alpha5 chain of collagen type IV. In conclusion, LEW recipients of F344 kidney grafts produce IgG1 antibodies against donor type perlecan and alpha1(VI)/alpha5(IV) collagen and develop transplant glomerulopathy. These data implicate an important role for the humoral immune response in the development of glomerulopathy during chronic rejection. (+info)The influence of the pericellular microenvironment on the chondrocyte response to osmotic challenge. (5/145)
OBJECTIVE: To examine whether differences in the pericellular microenvironment of different chondron preparations influence the chondrocyte volume regulatory response to experimental osmotic challenge. DESIGN: Mechanically extracted chondrons (MC), enzymatically extracted chondrons (EC) and isolated chondrocytes (IC) were seeded into agarose and sampled at 1, 3 and 7 days. Samples mounted in a perfusion chamber were subjected to osmotic challenge. The cross-sectional areas of the chondrocyte and pericellular microenvironment were measured under isotonic, hypertonic and hypotonic conditions, and percentage change calculated. Separate samples were immunolabeled for type VI collagen and keratan sulfate. RESULTS: Initially, the microenvironment of MC represented 60% of the chondron area and was occupied by type VI collagen and keratan sulfate. In EC, the microenvironment comprised 18% of the chondron area with narrow bands of type VI collagen and keratan sulfate. IC had no visible microenvironment, with small amounts of type VI collagen and keratan sulfate present. All preparations sequestered additional pericellular macromolecules during culture. Under isotonic conditions, the EC and IC chondrocytes were larger than those of MC. All chondrocytes shrank under hypertonic conditions and swelled under hypotonic conditions. MC were the least responsive, displaying the most efficient volume regulation. IC showed the largest response initially but this decreased with time. EC exhibited intermediate responses that decreased as the microenvironment increased in size. CONCLUSIONS: The composition and structural integrity of the pericellular microenvironment do influence the cellular response to experimental osmotic challenge. This suggests that the microenvironment functions in situ to mediate the chondrocyte response to physicochemical changes associated with joint loading. (+info)Mutations in COL6A3 cause severe and mild phenotypes of Ullrich congenital muscular dystrophy. (6/145)
Ullrich congenital muscular dystrophy (UCMD) is an autosomal recessive disorder characterized by generalized muscular weakness, contractures of multiple joints, and distal hyperextensibility. Homozygous and compound heterozygous mutations of COL6A2 on chromosome 21q22 have recently been shown to cause UCMD. We performed a genomewide screening with microsatellite markers in a consanguineous family with three sibs affected with UCMD. Linkage of the disease to chromosome 2q37 was found in this family and in two others. We analyzed COL6A3, which encodes the alpha3 chain of collagen VI, and identified one homozygous mutation per family. In family I, the three sibs carried an A-->G transition in the splice-donor site of intron 29 (6930+5A-->G), leading to the skipping of exon 29, a partial reduction of collagen VI in muscle biopsy, and an intermediate phenotype. In family II, the patient had an unusual mild phenotype, despite a nonsense mutation, R465X, in exon 5. Analysis of the patient's COL6A3 transcripts showed the presence of various mRNA species-one of which lacked several exons, including the exon containing the nonsense mutation. The deleted splice variant encodes collagen molecules that have a shorter N-terminal domain but that may assemble with other chains and retain a functional role. This could explain the mild phenotype of the patient who was still ambulant at age 18 years and who showed an unusual combination of hyperlaxity and finger contractures. In family III, the patient had a nonsense mutation, R2342X, causing absence of collagen VI in muscle and fibroblasts, and a severe phenotype, as has been described in patients with UCMD. Mutations in COL6A3 are described in UCMD for the first time and illustrate the wide spectrum of phenotypes which can be caused by collagen VI deficiency. (+info)Isolation of up- or down-regulated genes in PPARgamma-expressing NIH-3T3 cells during differentiation into adipocytes. (7/145)
Adipocyte differentiation is a complex process in which the expression of many transcription factors and adipocyte-specific genes is regulated under a strict program. The peroxisome proliferator-activated receptor gamma (PPARgamma), a member of the steroid/thyroid nuclear hormone receptor superfamily of ligand-activated transcription factors, is an important regulator of adipocyte gene expression and differentiation. In this study, we tried to identify downstream target genes of PPARgamma, by using PPARgamma-expressing cells and a subtractive cloning strategy, and isolated cDNA clones which were up-regulated or down-regulated by PPARgamma. Northern blot analyses revealed that the expression levels of the aldehyde dehydrogenase-2-like, type VI collagen alpha 3 subunit, cellular retinoic acid binding protein 1 and thrombospondin 1 are changed during the differentiation of mouse 3T3-L1 preadipocyte cells, indicating that these genes might be downstream targets of PPARgamma in adipocyte differentiation. (+info)Identification of known and novel genes whose expression is regulated by endogenous retinoic acid during early embryonic development of the mouse. (8/145)
Retinoic acid (RA) derived from vitamin A is necessary for, among other things, mammalian embryonic development. Although the impact of RA-dependent gene-regulation on embryonic development has been examined through genetic disruption of the retinoid receptors, the understanding of the underlying molecular mechanism remain unclear, in part, due to the difficulty in identifying RA-regulated genes in an intact embryo. We report here that RA-regulated genes can be identified from total RA-deficient embryos created by retinol-binding protein antisense (RBP-AS) oligodeoxynucleotide treatment in conjunction with differential display. Of the 28 genes isolated, 15 genes matched known genes in the GenBank database and the others either represented EST sequences or encoded novel genes. Semi-quantitative reverse transcriptase-polymerase chain reaction verified that the mRNA levels of mouse DN 38, COL VI 3 alpha, cul-1, alpha-tropomyosin, and PP2A-C alpha were substantially increased, whereas mouse Msh 2, Ndufa2, Ribosomal protein S19, sFRP-1, GDAP-10 and mSmcD were significantly decreased in vitamin A deficient (VAD) embryos compared to the control embryos. The utility of the method is exemplified by our finding that several genes in the Wnt signaling pathway are vitamin A regulated in day 9.0 post coitum (p.c.) embryos. (+info)Symptoms of MPS VI typically become apparent in the first year of life and can include:
* Coarsening of facial features
* Enlarged liver and spleen
* Short stature
* Joint stiffness and progressive joint degeneration
* Corneal clouding
* Sleep apnea
* Heart valve problems
* Respiratory difficulties
MPS VI is diagnosed through a combination of physical examination, medical history, and laboratory tests, including enzyme assays and genetic analysis. There is currently no cure for MPS VI, but various treatments are available to manage the symptoms and improve quality of life. These may include:
* Enzyme replacement therapy (ERT) to replace the missing NAGLU enzyme
* Bone marrow transplantation to correct the genetic defect and restore normal enzyme function
* Physical therapy to maintain joint mobility and prevent contractures
* Respiratory support to manage breathing difficulties
* Cardiac monitoring and treatment to address heart valve problems
Early diagnosis and appropriate management of MPS VI can help to improve the quality of life for affected individuals, but it is important to note that this condition is a lifelong condition and ongoing medical care will be necessary.
Symptoms of GSD VI typically appear during infancy or early childhood and may include:
* Delayed development and growth
* Poor muscle tone and weakness
* Increased risk of hypoglycemia (low blood sugar)
* Liver enlargement
* Yellowing of the skin and eyes (jaundice)
* Increased risk of infections and other health problems.
GSD VI is diagnosed through a combination of clinical evaluation, laboratory tests, and genetic analysis. Treatment for the condition typically involves a high-carbohydrate diet, regular monitoring of blood sugar levels, and managing any associated health problems. In some cases, liver transplantation may be necessary.
Glycogen storage disease type VI is a rare and debilitating disorder that can significantly impact the quality of life of affected individuals and their families. It is important to work with a team of healthcare professionals to manage the condition and provide appropriate support and resources.
Collagen, type VI, alpha 1
Collagen, type VI, alpha 3
Collagen, type VI, alpha 2
Collagen, type VI, alpha 5
Collagen, type IV, alpha 6
Collagen VI
Collagen, type XV, alpha 1
Collagen, type VII, alpha 1
Collagen, type XI, alpha 1
Collagen, type XXVIII, alpha 1
Collagen, type II, alpha 1
Collagen, type IV, alpha 1
Collagen, type XII, alpha 1
Collagen, type XVI, alpha 1
Collagen, type I, alpha 2
Collagen loss
Collagen, type IX, alpha 3
Collagen, type IX, alpha 1
Collagen, type IX, alpha 2
Collagen, type XXIII, alpha 1
Collagen, type VIII, alpha 1
Collagen, type XIII, alpha 1
Collagen, type XXVII, alpha 1
Collagen, type V, alpha 3
Collagen, type IV, alpha 2
Type II collagen
Collagen, type I, alpha 1
Collagen, type IV, alpha 5
Collagen, type XIX, alpha 1
Collagen, type XIV, alpha 1
Catenin
Equine anatomy
Topical fluoride
Fibroblast-like synoviocyte
ABL (gene)
Senescence
Anti-aging product
Achilles tendinitis
Paleolithic
List of diseases (C)
Harvey Cantor
Koenen's tumor
Integrin alpha 2
Striated muscle tissue
Trimeric autotransporter adhesin
Charles M. Russell National Wildlife Refuge
LECT2
Diagenesis
Pseudolysin
Sprain
Stress incontinence
Liposuction
Signaling peptide receptor
AP-1 transcription factor
Liver support system
Glaucoma
CUTL1
Primary effusion lymphoma
Bioarchaeology
The Role of Type VI Collagen in Alveolar Bone. | Int J Mol Sci;23(22)2022 Nov 18. | MEDLINE | BVS Odontologia
Type XVII Collagen Regulates Lamellipod Stability, Cell Motility, and Signaling to Rac1 by Targeting Bullous Pemphigoid Antigen...
Ultra collagen type 1 &3 Calories, Carbs & Nutrition Facts | MyFitnessPal
Collagen VI-related dystrophy: MedlinePlus Genetics
Anti-Collagen IV antibody (ab6586) | Abcam
Pathophysiology and Etiology
Chromosome 6 - wikidoc
Kromosomang 6 (tao) - Wikipedia, ang malayang ensiklopedya
A biomimetic engineered bone platform for advanced testing of prosthetic implants | Scientific Reports
MMRRC:039746-MU
WHO EMRO | Serum endostatin and vascular endothelial growth factor levels in patients with pre-eclampsia | Volume 12, issue 1...
WHO EMRO | Serum endostatin and vascular endothelial growth factor levels in patients with pre-eclampsia | Volume 12, issue 1...
Combination of stromal cell-derived factor-1 and collagen-glycosaminoglycan scaffold delays contraction and accelerates...
Autoantibodies as Diagnostic Markers and Mediator of Joint Inflammation in Arthritis
Identification of Molecules in Leech Extracellular Matrix that Promote Neurite Outgrowth - NASA/ADS
NIOSHTIC-2 Search Results - Full View
In New Era of Gene Therapy, PCPs Are 'Boots on the Ground'
Hepatocyte growth factor attenuates collagen accumulation in a murine model of pulmonary fibrosis
Alport Syndrome: Practice Essentials, Background, Pathophysiology and Etiology
PDO Thread Lift Procedure, Benefits, and Side Effects
Frequency of clonal intraepithelial T lymphocyte proliferations in enteropathy-type intestinal T cell lymphoma, coeliac disease...
Dietary supplements for treating osteoarthritis: a systematic review and meta-analysis | British Journal of Sports Medicine
Enea Ferlizza - University of Bologna - Publications
Benefits of Aloe Vera
Purdue e-Pubs - Society of Engineering Science 51st Annual Technical Meeting: Strain rate hardening in biological and...
JCI -
Probiotic/prebiotic supplementation of antiretrovirals improves gastrointestinal immunity in SIV-infected macaques
Collasate Postoperative and Wound Dressing: Wound Care for Pets
Effect of royal jelly ingestion for six months on healthy volunteers | Nutrition Journal | Full Text
Mutations10
- Variants (also known as mutations) in the COL6A1 , COL6A2 , and COL6A3 genes can cause the various forms of collagen VI-related dystrophy. (medlineplus.gov)
- Patients with recessive dystrophic epidermolysis bullosa (RDEB) have incurable skin fragility, blistering, and skin wounds due to mutations in the gene that codes for type VII collagen (C7) that mediates dermal-epidermal adherence in human skin. (nih.gov)
- Mutations in these genes result in abnormalities of the type IV collagen in glomeruli, which prevents the kidneys from properly filtering the blood and allows blood and protein to pass into the urine. (nih.gov)
- Mutations that disrupt type IV collagen can result in misshapen lenses and an abnormally colored retina. (nih.gov)
- Certain gene changes, or mutations, cause the collagen defects. (nih.gov)
- About 80%-90% of OI cases are caused by autosomal dominant mutations in the type 1 collagen genes, COL1A1 and COL1A2 . (nih.gov)
- Mutations in one or the other of these genes cause the body to make either abnormally formed collagen or too little collagen. (nih.gov)
- Mutations in these genes cause OI Types I through IV. (nih.gov)
- The remaining cases of OI (types VI-XI) are caused by autosomal recessive mutations in any of six genes ( SERPINF1, CRTAP, LEPRE1, PPIB, SERPINH1, and FKBP10 ) that code for proteins that help make collagen. (nih.gov)
- These mutations also cause the body to make too little collagen or abnormally formed collagen. (nih.gov)
Gene6
- This invention includes the identification of a new mutation in the collagen type VI (COL6A1) gene, including a method for diagnosing and treating patients with this mutation. (nih.gov)
- Our novel identification includes a mutation in intron 11 of the COL6A1 gene that alters the splicing of the gene pre-mRNA and produces a mature alpha 1 (VI) chain mRNA that comprises an additional exon. (nih.gov)
- The human leukocyte antigen lies on chromosome 6, with the exception of the gene for β2-microglobulin (which is located on chromosome 15 ), and encodes cell-surface antigen -presenting proteins among other functions. (wikidoc.org)
- Ang kromosomang 6 ay malamang na naglalaman sa pagitan ng 2,000 at 2,057 na mga gene. (wikipedia.org)
- BACKGROUND Clonal T cell receptor (TCR) gene rearrangements and loss of T cell antigens such as CD8 and TCR-β in intraepithelial lymphocytes (IELs) may indicate the development of an enteropathy-type intestinal T cell lymphoma (EITCL) in patients with refractory sprue. (bmj.com)
- RESULTS Clonal TCR-γ gene rearrangements were found in all resected tumours of patients with EITCL, in 3/8 duodenal biopsies of patients with EITCL, in 2/2 patients with ulcerative jejunitis, in 2/3 patients with refractory sprue evolving into overt EITCL, and in 1/6 patients with refractory sprue. (bmj.com)
Antigen1
- Intratracheal administration of 100 micrograms of rhHGF to C57BL/6 mice led to proliferation of bronchial and alveolar epithelial cells as indicated by an increased number of cells staining for proliferating cell nuclear antigen (PCNA). (nih.gov)
Integrin1
- Moreover, diabetic renal ECM shows diminished binding of α1β1 integrin consistent with the modification of collagen IV by hypochlorous (HOCl) and hypobromous acids. (diabetesjournals.org)
Chromosome7
- Human chromosome 6 pair after G-banding . (wikidoc.org)
- Chromosome 6 pair in human male karyogram . (wikidoc.org)
- Chromosome 6 is one of the 23 pairs of chromosomes in humans . (wikidoc.org)
- Chromosome 6 spans more than 170 million base pairs (the building material of DNA ) and represents between 5.5 and 6% of the total DNA in cells . (wikidoc.org)
- In 2003, the entirety of chromosome 6 was manually annotated for proteins, resulting in the identification of 1,557 genes, and 633 pseudogenes . (wikidoc.org)
- The following is a partial list of genes on human chromosome 6. (wikidoc.org)
- Chromosome 6 ) ang isa sa mga 23 pares ng mga kromosoma sa mga tao . (wikipedia.org)
Make collagen1
- The defect in the genes causes the body to make collagen incorrectly or not make enough, leading to weak bones that break more easily. (nih.gov)
COL6-RD2
- Collagen type VI-related dystrophies (COL6-RD) are devastating neuromuscular disorders that manifest with progressive generalized muscle weakness, contractures, and respiratory failure. (nih.gov)
- Collagen 6-related dystrophies and myopathies (COL6-RD) are a group of disorders that form a wide phenotypic spectrum, ranging from severe Ullrich congenital muscular dystrophy, intermediate phenotypes, to the milder Bethlem myopathy. (ru.nl)
Hydrolysate5
- A portion of the hydrolysate was analyzed for hydroxyproline using high performance liquid chromatography with collagen type I as the standard. (cdc.gov)
- All Collasate products contain Medical Hydrolysate of Type 1 Collagen. (vetrxdirect.com)
- Collasate Postoperative Dressing ingredients: Medical Hydrolysate of Type I Collagen. (vetrxdirect.com)
- Collasate Spray ingredients: Medical Hydrolysate of Type I Collagen, Bitrex, and collascent. (vetrxdirect.com)
- Collasate Silver ingredients: Medical Hydrolysate of Type I Collagen, 1% Silver Oxide. (vetrxdirect.com)
C57BL1
- C57BL/6 mice with 1 cm × 1 cm dorsal full-thickness wounds were covered with a collagen-glycosaminoglycan scaffold, followed by four daily topical applications of 1 μg SDF-1 or phosphate-buffered saline vehicle. (harvard.edu)
Extracellular6
- Type VI collagen makes up part of the extracellular matrix that surrounds muscle cells and connective tissue. (medlineplus.gov)
- Research suggests that type VI collagen helps secure and organize the extracellular matrix by linking the matrix to the cells it surrounds. (medlineplus.gov)
- Changes in type VI collagen structure or production lead to an unstable extracellular matrix that is no longer attached to cells. (medlineplus.gov)
- Non-specific cross reaction of anti-collagen antibodies with other human serum proteins or non-collagen extracellular matrix proteins is negligible. (abcam.com)
- Immunoaffinity chromatography using immobilized antigens followed by extensive cross-adsorption against other collagens, human serum proteins and non-collagen extracellular matrix proteins to remove any unwanted specificities. (abcam.com)
- Mature human SCARA5 consists of a 60 amino acid (aa) cytoplasmic domain, a 21 aa transmembrane segment, and a 414 aa extracellular domain (ECD) with a spacer, a collagen-like, and a scavenger receptor cysteine-rich (SRCR) domain (4-6). (rndsystems.com)
Dystrophies1
- Collagen VI (COL6) is known for its role in a spectrum of congenital muscular dystrophies, which are often accompanied by respiratory dysfunction. (nih.gov)
Genes3
- These genes each provide instructions for making one component of a protein called type VI collagen. (medlineplus.gov)
- Variants in the COL6A1 , COL6A2 , and COL6A3 genes result in a decrease or lack of type VI collagen or the production of abnormal type VI collagen. (medlineplus.gov)
- For most people, a change or defect in the genes that carry the instructions for making type I collagen causes OI. (nih.gov)
20161
- Epub 2016 Dec 6. (nih.gov)
Protein called type1
- OI is caused by defects in or related to a protein called type 1 collagen. (nih.gov)
Abnormalities2
Hydroxyproline2
- We found that HGF significantly attenuated collagen accumulation induced by bleomycin as determined by quantitation of hydroxyproline content and by scoring of the extent of fibrosis. (nih.gov)
- Analysis of hydroxyproline (collagen) and pyridinoline (collagen cross-links) in biopsies prepared for routine histological evaluation with OCT compound was performed. (cdc.gov)
Chondroitin2
- Chondroitin sulfate is likely safe when used for up to 6 years. (nih.gov)
- Another six (undenatured type II collagen, avocado soybean unsaponifiables, methylsulfonylmethane, diacerein, glucosamine and chondroitin) revealed statistically significant improvements on pain, but were of unclear clinical importance. (bmj.com)
COL6A11
- Parental mosaicism was confirmed in the four families through quantitative analysis of the ratio of mutant versus wild-type allele (COL6A1, COL6A2, and COL6A3) in genomic DNA from various tissues, including blood, dermal fibroblasts, and saliva. (ru.nl)
Antibodies1
- These autoantibodies (anticitrullinated protein/peptide antibodies (ACPAs), rheumatoid factors (RF), anticollagen type II antibodies, antiglucose-6 phosphate isomerase antibodies, anticarbamylated protein antibodies, and antiacetylated protein antibodies) have different characteristics, diagnostic/prognostic value, and pathological significance in RA patients. (hindawi.com)
Recombinant1
- There are other recombinant monoclonal options, such as Recombinant Anti-Collagen IV antibody . (abcam.com)
Subunit1
- ab6586 is designed to bind specifically to NATIVE collagen epitopes composed of multiple subunit strands. (abcam.com)
Proteins1
- Class A scavenger receptors, including CL-P1, MARCO, SCARA3, and SR-A1, are type II transmembrane proteins that contain a collagenous stalk (1-3). (rndsystems.com)
Consistent3
- These were accompanied by the reduced expression of connective tissue growth factor, fewer α smooth muscle actin (α-SMA)-positive myofibroblasts, and less deposition of collagen in the healed neodermis, consistent with less scar formation. (nih.gov)
- Collagen concentration increased by five-fold and collagen cross-links by more than 7-fold consistent with fibrotic changes known to occur with denervation. (cdc.gov)
- Consistent with somatic mosaicism, parental samples had lower ratios of mutant versus wild-type allele compared with the fully heterozygote offspring. (ru.nl)
Alveolar2
- The Role of Type VI Collagen in Alveolar Bone. (bvsalud.org)
- In conclusion, Type VI collagen has a role in controlling biomineralization in alveolar bone and that changes in the ECM of alveolar bone could be associated with greater bone loss due to periodontitis . (bvsalud.org)
Clinically2
19961
- 1996) Evaluation of different chemical methods for cros-linking collagen gel, films and sponges. (aimspress.com)
Chain2
- Structure and multiple conformations of the Kunitz-type domain from human type VI collagen alpha 3(VI) chain in solution. (nih.gov)
- The compaction of collagen films, mediated by the drying and cross-linking fabrication process, suggests a less open organization compared to native fibrillar collagen that likely allowed the collagen to form more inter-chain bonds and chemical links with NDGA polymers. (aimspress.com)
Biopsies1
- In addition, biopsies from six consecutive patients with refractory sprue of uncertain cause were examined. (bmj.com)
Analyze2
Cells2
- 6. Type IV collagen induces STAT5 activation in MCF7 human breast cancer cells. (nih.gov)
- The presence of these sutures in your skin triggers cells in your body called fibroblasts to produce more collagen . (healthline.com)
Bones2
Mice2
- Herein, we examined the effect of the chemokine stromal cell-derived factor-1 (SDF-1) on the performance of a porous collagen-glycosaminoglycan dermal analog in excisional wounds in mice. (harvard.edu)
- The effect of HGF on the lung repair process was examined by administration of 100 micrograms of rhHGF on Day 3 and Day 6 after intratracheal injection of bleomycin to mice. (nih.gov)
Noncollagenous2
- Endostatin is derived from the noncollagenous domain 1 (NC1) at the C-terminus of collagen type XVIII. (who.int)
- Noncollagenous (NC1) hexamers, key connection modules of collagen IV networks, are modified via oxidation and chlorination of tryptophan and bromination of tyrosine residues. (diabetesjournals.org)
Concentration3
- Nous avons déterminé la concentration d'endostatine et de VEGF dans le sérum de 20 femmes non enceintes en bonne santé et de 64 femmes enceintes : 20 en bonne santé, 20 ayant une prééclampsie bénigne et 24 une prééclampsie grave. (who.int)
- La concentration sérique pour ces facteurs chez les femmes non enceintes était similaire à celle des femmes enceintes en bonne santé. (who.int)
- Toutefois, la concentration sérique était significativement plus élevée en présence d'une prééclampsie bénigne ou grave par rapport aux grossesses normales et significativement plus élevée pour les prééclampsies graves par rapport aux prééclampsies bénignes. (who.int)
Wound2
- Wound Repair and Regeneration 19 (1) (December 6): 71-79. (harvard.edu)
- Unlike other collagen products, which are made from native collagen, Collasate's hydrolyzed collagen is a patented product available in amino acid form to be immediately utilized by the wound site for healing, helping speed recovery. (vetrxdirect.com)
Results3
- However, there was a noticeable decline in results 6 months later. (healthline.com)
- Most severe type among those who survive the neonatal period and usually results in the greatest number of physical disabilities. (nih.gov)
- Our results suggest that hypohalous acid-derived modifications of renal ECM, and specifically collagen IV networks, contribute to functional protein damage in diabetes. (diabetesjournals.org)
Severe3
- Researchers have described several forms of collagen VI-related dystrophy, which range in severity: Bethlem muscular dystrophy is the mildest, an intermediate form is moderate in severity, and Ullrich congenital muscular dystrophy is the most severe. (medlineplus.gov)
- While it is difficult to predict which type of variant will lead to which form of collagen VI-related dystrophy, in general, lower amounts of type VI collagen lead to more severe signs and symptoms that begin earlier in life. (medlineplus.gov)
- Type II is the most severe form of OI. (nih.gov)
Liver1
- Collagen concentrations ranged from 6.6 microg/mg dry weight (liver) to 74.7 microg/mg dry weight (diaphragm). (cdc.gov)
Tendon3
- Many studies have been conducted to elucidate the role of Type VI collagen in muscle and tendon , however, its role in oral tissues remains unclear. (bvsalud.org)
- Fixation is required to reinforce reconstituted collagen for orthopedic bioprostheses such as tendon or ligament replacements. (aimspress.com)
- Type I collagen is also in other connective tissues such as tendon, ligament, lung, and skin, and these tissues can sometimes be affected. (nih.gov)
Human1
- Collagen Type IV from human and bovine placenta. (abcam.com)
Humans1
- Six-month ingestion of RJ in humans improved erythropoiesis, glucose tolerance and mental health. (biomedcentral.com)
Structure2
- Collagen is the protein that gives your skin its structure and elasticity. (healthline.com)
- Normal collagen structure, but less than the normal amount is produced. (nih.gov)
Evaluation1
- Effect of nordihydroguaiaretic acid cross-linking on fibrillar collagen: in vitro evaluation of fibroblast adhesion strength and migration[J]. AIMS Bioengineering, 2017, 4(2): 300-317. (aimspress.com)
Form3
- The intermediate form of collagen VI-related dystrophy is characterized by muscle weakness that begins in infancy. (medlineplus.gov)
- Type I is the mildest and most common form of OI. (nih.gov)
- Medical grade gel form of collagen. (vetrxdirect.com)
Coeliac1
- Enteropathy-type intestinal T cell lymphoma (EITCL) is a complication of longstanding and untreated coeliac disease. (bmj.com)
Domain1
- Alternate splicing generates isoforms that lack the SRCR domain, the transmembrane segment, or the 225 aa spacer region between the membrane and the collagen-like domain (6). (rndsystems.com)
Migration1
- This work focuses on investigating fibroblast behavior on fibrillar and NDGA cross-linked type I collagen to determine if NDGA modulates cell adhesion, morphology, and migration. (aimspress.com)
Loss3
- Alterations in type IV collagen often result in abnormal inner ear function, which can lead to hearing loss. (nih.gov)
- its loss enhances angioge-nesis and vascular permeability [6]. (who.int)
- Loss of collagen is one of the main causes of aging skin. (healthline.com)
Production2
- Smooth sutures that help rejuvenate your skin by stimulating collagen production. (healthline.com)
- They last longer in your body and tend to stimulate more collagen production. (healthline.com)