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Topic: Collagen VII

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	Collagen - Wikipedia, the free encyclopedia
		Collagen means "glue producer" (kolla is Greek for glue), derived from the early process of boiling the skin and sinews of horses and other animals to obtain glue.
		Collagens are still employed in the construction of artificial skin substitutes used in the management of severe burns.
		Type III collagen - This is the collagen of granulation tissue, and is produced quickly by young fibroblasts before the tougher type I collagen is synthesized.
	en.wikipedia.org /wiki/Collagen (1427 words)

	COL7A1 - collagen, type VII, alpha 1 (epidermolysis bullosa, dystrophic, dominant and recessive)
		Since type VII collagen is the major component of the anchoring fibrils, we examined the genetic linkage of dominant dystrophic EB (EBDD) and the type VII collagen gene (COL7A1) locus, which we have recently mapped to chromosome 3p, in three large kindreds with abnormal anchoring fibrils.
		Mutations in the COL7A1 gene encoding collagen VII have been disclosed in a number of DEB families, and the mutation analyses and studies on genotype-phenotype correlations in DEB have revealed an unusual complexity of the gene defects and their biological consequences.
		The collagen VII gene, COL7A1, is the candidate gene for both the recessive and dominant forms of dystrophic epidermolysis bullosa (EBD).
	www.ihop-net.org /UniPub/iHOP/gi/87334.html (5180 words)

	What is Collagen? (Site not responding. Last check: 2007-10-20)
		Collagens in was a barrier to study until it was found that tropocollagen from young animals can be extracted because it is not yet fully.
		Collagen injections are generally off limits for pregnant women, individuals who are allergic to beef or bovine products, patients who suffer from autoimmune diseases, and those who are allergic to lidocaine (the anesthetic agent contained in the syringe with the collagen material).
		Collagen is a naturally occurring protein that provides support to various parts of the human body: the skin, the joints, the bones and the ligaments.
	collagen.bfind.info (2343 words)

	Epidermolysis bullosa - Wikipedia, the free encyclopedia
		The disease DEB is caused by genetic defects (or mutations) within the molecule type VII collagen (collagen VII).
		Collagen VII is a very large molecule (780 nm) that dimerizes to forms a semicircular looping structure: the anchoring fibril.
		Collagen VII is also present in the epithelial tissue of the esophagus, which leads to chronic scarring, webbing, and obstruction.
	en.wikipedia.org /wiki/Epidermolysis_bullosa (535 words)

	Equine Laminitis Basement Membrane Pathology: Loss of Type / V Collagen, Type VII Collagen and Laminin Immunostaining
		Disintegration of the basement membrane (BM) of the equine hoof lamellae and failure of the BM to remain attached to the basal cells of the secondary epidermal lamellae (SEL) is one of the earliest pathological events to occur in acute laminitis.
		Disintegration of the basement membrane (BM) of the hoof lamellae and failure of the BM to remain attached to the basal cells of the secondary epidermal lamellae (SEL) is one of the earliest pathological events to occur in acute laminitis (Pollitt 1996).
		The reaction with antibodies to type VII collagen establishes unequivocally that the membrane of the dilatations is lamellar and not vascular in origin, as type V11 collagen is not present in blood vessels and the lamellar vasculature never reacted with antibodies to type V11 collagen.
	www.horseshoes.com /advice/laminitis/lamininimmunostaining/lamininimmunostaining.htm (4804 words)

	All That Anchors
		Woodley was helped by his previous efforts in the field: In 1992, he and his colleagues became the first team to clone the human gene for type VII collagen, one of the key components of the skin’s extracellular matrix.
		Collagen makes up the tendrils and fibrils that provide a cushion for the skin’s cells to rest upon; type VII collagen, in particular, is critical to the creation of the skin’s so-called anchoring fibrils.
		Ever since their successful cloning of the type VII collagen gene, Woodley and Keck School associate professors of research Mei Chen and Wei Li, with gene therapy expert Nori Kasahara of USC’s Institute for Genetic Medicine, have been working to insert that gene into cells that are missing it.
	www.usc.edu /uscnews/stories/8567.html (617 words)

	Bio-engineered mouse produces human collagen: a step toward possible treatment of human disease
		Woodley was helped by his previous efforts in the field: In 1992, he and some of his colleagues became the first team to clone the human gene for type VII collagen, one of the key components of the skin’s extracellular matrix.
		Ever since their successful cloning of the type VII collagen gene, Woodley, along with Keck School of Medicine associate professors of research Mei Chen and Wei Li, as well as gene therapy expert Nori Kasahara from the Institute for Genetic Medicine, have been working to insert that gene into cells that are missing it.
		They have been able to get the collagen gene into both fibroblasts (the cells that normally produce collagen and other fibrous tissues) and keratinocytes (the cells which normally differentiate to form the outmost layer of skin).
	www.usc.edu /uscnews/stories/8561.html (630 words)

	USC researchers use gene therapy to prompt mouse cells to produce human collagen
		Los Angeles, Dec. 23——Researchers at the Keck School of Medicine of the University of Southern California, along with colleagues from across the country, have for the first time genetically engineered mouse cells to produce a type of human collagen--type VII--that is missing in a family of inherited skin diseases called dystrophic epidermolysis bullosa.
		Woodley was helped by his previous efforts in the field: In 1992, he and some of his colleagues became the first team to clone the human gene for type VII collagen, which is one of the key components of the skin's extracellular matrix.
		In subsequent work, Woodley adds, the engineered cells have shown that they are capable of continuing to pump out type VII collagen for at least six months--but so far, they have only done so in lab dishes.
	www.eurekalert.org /pub_releases/2002-12/uosc-uru122302.php (589 words)

	Research - Department of Dermatology - Stanford University School of Medicine
		Collagens are a normal part of the body and have not been appreciated to play a primary role in causing cancer.
		Cells from RDEB patients that retain a portion of collagen VII were recently observed to form experimentally-induced tumors in the laboratory at similar rates to cells from normal patients.
		Further studies are necessary to define the role of collagens in cancer and to see if collagen abnormalities combine with the chronic wounding seen in RDEB to increase the risk of cancer in RDEB patients.
	dermatology.stanford.edu /research/research.html (1596 words)

	Skin Inc. magazine Information \| News \| Protein Key to Skin Cancer Spread Found (Site not responding. Last check: 2007-10-20)
		The protein is collagen VII, one of a family of molecules that play an essential role in skin culture, says a report in the March 18 issue of Science by researchers at the Stanford University School of Medicine.
		Collagen VII normally keeps the outer layer of the skin anchored to the inner layer.
		At least a fragment of collagen VII is required for skin cancer cells to break free and start their potentially deadly spread, Khavari said.
	www.skininc.com /news/1397632.html (577 words)

	eMedicine Online Medical Textbooks by Specialty: Free Journal Articles and Texts for Physicians and Health Professionals
		NEW YORK (Reuters Health) - Collagen VII is needed for the tumor-stroma interactions that promote Ras-driven skin cancer, according to a report in the March 18th issue of Science.
		Defects in type VII collagen are known to cause recessive dystrophic epidermolysis bullosa (RDEB), a blistering skin disease that is often associated with epidermal cancers.
		To investigate the role collagen VII plays in these malignancies, Dr. Paul A. Khavari, from Stanford University School of Medicine in California, and colleagues examined Ras-driven tumor formation in RDEB skin cells.
	www.emedicine.com /news.asp?name=20050317scie003.xml&page=Neurology (286 words)

	eMedicine - Epidermolysis Bullosa Acquisita : Article Excerpt by: Lawrence Chan, MD (Site not responding. Last check: 2007-10-20)
		Immunologically, EBA is characterized by the presence of immunoglobulin G (IgG) autoantibodies (in most patients) targeting the noncollagenous (NC1) domain of type VII collagen, the major component of anchoring fibrils that connect the basement membrane to dermal structures.
		IgG autoantibodies specific for anchoring fibrils (type VII collagen) of the skin basement membrane have a heterogeneous subclass and light chain composition, and their complement-activating capacities do not correlate with the inflammatory phenotype.
		Passive transfer of antibodies raised in rabbits against mouse type VII collagen induced blister formation in mice, thus confirming the potential role of antitype VII collagen antibody in the pathogenesis of the disease.
	www.emedicine.com /derm/byname/epidermolysis-bullosa-acquisita.htm (592 words)

	Epidermolysis bullosa acquisita
		The patients' anti-type VII collagen autoantibodies, likely to be polyclonal in nature, may contribute to the pathogenesis of the blistering process by both complement-dependent inflammatory injury and complement-independent mechanical disruption of the anchoring function of type VII collagen.
		Epidermolysis bullosa acquisita (EBA) is a rare, immunobullous disease, characterized by circulating and tissue-bound antibodies against type VII collagen (C7) of anchoring fibrils in the cutaneous basement membrane zone.
		Epidermolysis bullosa acquisita (EBA) is an autoimmune subepidermal blistering disease characterized by IgG anti-basement membrane autoantibodies to collagen VII.
	www.thedoctorsdoctor.com /diseases/epidermolysis_bullosa_acquisita.htm (7877 words)

	NCI HTML Cancer Bulletin for April 5, 2005 - National Cancer Institute
		The research team from Stanford University School of Medicine worked with skin keratinocytes and skin cancers from patients with the genetic disease recessive dystrophic epidermolysis bullosa (RDEB), in whom the collagen VII gene is mutated, causing their skin to be fragile and blister.
		The authors showed that physical interactions between collagen VII and laminin-5, an extracellular basement membrane protein, facilitates SCC invasion, and further demonstrated that an N-terminal fragment of collagen VII, FNC1, was sufficient for tumor formation and invasion.
		The authors propose that collagen VII or FNC1 may be a novel therapeutic target against tumor invasion.
	www.cancer.gov /ncicancerbulletin/NCI_Cancer_Bulletin_040505/page5 (1393 words)

	What's New
		What Khavari and postdoctoral scholar Susana Ortiz-Urda, MD, PhD, found is that a fragment of collagen VII is required for the skin cancer cells to break free from the neighboring skin tissue and spread - a step that turns an otherwise benign tumor into a killer.
		Khavari and his group deduced that this collagen VII protein fragment might be necessary to allow cancer to form.
		Khavari said he could imagine a drug that blocks the collagen VII fragment being used pre-emptively to prevent skin cancer from spreading in people who are highly susceptible, such as children with RDEB or people who are chronically immune suppressed due to organ transplantation.
	www.acor.org /news/whatsnew.html?item_id=3164 (740 words)

	Modified Basement Membrane Composition During Bronchopulmonary Tumor Progression -- Catusse et al. 48 (5): 663 -- ...
		VII collagen (at a concentration of 10 µg/ml).
		The anti-LN5 (Lane 6) and the anti-Type VII collagen (Lane 7) antibodies detect, respectively, one band at 200 kD and one band at 240 kD in tumor tissue extracts.
		Sakai LY, Keene DR, Burgesson RE (1986) Type VII collagen is a major structural component of anchoring fibrils.
	www.jhc.org /cgi/content/full/48/5/663 (3012 words)

	Laminin 5 Binds the NC-1 Domain of Type VII Collagen -- Rousselle et al. 138 (3): 719 -- The Journal of Cell Biology
		To be certain that the binding of laminin 5 to type VII collagen NC-1 was not artifactually influenced by the solid-phase
		VII collagen can be seen on some NC-1 molecules.
		The relationship of the biophysical and biochemical characteristics of type VII collagen to the function of anchoring fibrils.
	www.jcb.org /cgi/content/full/138/3/719 (6547 words)

	[No title]
		Type II collagen - Articular cartilage Type III collagen - This is the collagen of HYPERLINK "http://en.wikipedia.org/w/index.php?title=Granulation_tissue&action=edit" \o "Granulation tissue" granulation tissue, and is produced quickly by young fibroblasts before the tougher type I collagen is synthesised.
		major collagen found in skin, tendon, bone, dentin; a fetal form also exists Mutations in the cleaving of the procollagen I have been shown to be responsible for Ehrlers-Danlos syndrome type VII, a disorder characterized by extreme joint hypermobility and congenital bilateral hip dislocations.
		Other mutations in collagen I produce osteogenesis imperfecta, a highly variable condition (depending on the place of the mutation) characterized by deformed bones, short stature, and abnormalities of teeth.
	cim.ucdavis.edu /classpages/2008/newstudyaids/anatomy/14marciacollagen.doc (661 words)

	Tumorigenesis: The collagen connection - Cell Signaling Update - Signaling Gateway
		Functional defects in type VII collagen are responsible for RDEB, and Susana Ortiz-Urda and colleagues have disovered that SCC development in these patients is dependent on collagen-VII-mediated interactions between the tumour and its microenvironment.
		The two populations could be further distinguished by the expression of collagen VII: primary keratinocytes from patients with tumorigenic RDEB express a portion of collagen VII, whereas the cells from the non-tumorigenic RDEB subset (termed RDEB
		But the authors suggest that as collagen VII and laminin-5 are extracellular, they will in principle be accessible to therapeutics such as antibodies.
	www.signaling-gateway.org /update/updates/200505/nrc1615.html (460 words)

	Establishment of an Animal Model for
		Biochemical analysis by limited proteolysis of the recombinant polypeptides using pepsin or collagenase confirmed that the recombinant collagen type VII was secreted as a correctly-folded helical trimer preserving the functional domains of the wild-type counterpart (this part of the work was done in collaboration with Dr. Bruckner-Tuderman, Münster, Germany).
		The synthesis and expression pattern of the recombinant collagen type VII in in vitro reconstructed skin was assessed using organotypic cultures.
		Immunohistochemical analysis of the reconstructed skin showed that the immunoreactive recombinant collagen type VII was detected at the basement membrane of the dermal-epidermal junction of the artificial skin tissue.
	www.debra-international.org /a_mengusi3a.htm (673 words)

	Induction of dermal-epidermal separation in mice by passive transfer of antibodies specific to type VII collagen -- ...
		Schematic organization of human type VII collagen and cDNA constructs generated for this study for expressing recombinant peptides of the NC1 domain.
		Autoantibodies to type VII collagen recognize epitopes in a fibronectin-like region of the noncollagenous (NC1) domain.
		Type VII collagen is a normal component of epidermal basement membrane, which shows altered expression in recessive dystrophic epidermolysis bullosa.
	www.jci.org /cgi/content/full/115/4/870 (6080 words)

	Dystrophic
		The possible pathogenicity of skin collagenase in RDEB was further supported by the intriguing observation by Bauer and colleagues in 1980 that the treatment of a series of RDEB patients with systemic phenytoin led both to a reduction in blister counts and to the reduced synthesis of collagenase by dermal fibroblasts from these patients.
		Mutations are noted in the genes encoding collagen VII either the gene from the mother or from the father.
		Some affected by this form of EB may note the presence of small, firm flesh colored or white skin elevations that appear spontaneously on the trunk and extremeties of their body, that are called albopapuloid lesions.
	www.homestead.com /ebinfo/Dystrophic.html (2538 words)

	Autoantibodies to Type VII Collagen Mediate Fc{gamma}-Dependent Neutrophil Activation and Induce Dermal-Epidermal ...
		Autoantibodies to type VII collagen from EBA serum were purified using a recombinant form of the NC1 domain covalently coupled to an agarose matrix.
		Dermal-epidermal separation is dependent on the Fc portion of autoantibodies to type VII collagen.
		VII collagen from EBA patients and of a monoclonal antibody
	ajp.amjpathol.org /cgi/content/full/161/1/301 (4825 words)

	Publication Details - Paul A. Khavari, MD, PhD - Stanford University School of Medicine
		Type VII collagen defects cause recessive dystrophic epidermolysis bullosa (RDEB), a blistering skin disorder often accompanied by epidermal cancers.
		Cells devoid of collagen VII did not form tumors in mice, whereas those retaining a specific collagen VII fragment (the amino-terminal noncollagenous domain NC1) were tumorigenic.
		Tumor-stroma interactions mediated by collagen VII thus promote neoplasia, and retention of NC1 sequences in a subset of RDEB patients may contribute to their increased susceptibility to squamous cell carcinoma.
	www-med.stanford.edu /profiles/frdActionServlet?choiceId=showPublication&pubid=54465&fid=4683 (184 words)

	Protein that binds skin cells found to play vital role in spread of skin cancer
		What Khavari and postdoctoral scholar Susana Ortiz-Urda, MD, PhD, found is that a fragment of collagen VII is required for the skin cancer cells to break free from the neighboring skin tissue and spread—a step that turns an otherwise benign tumor into a killer.
		It turns out that the difference in cancer formation had to do with the type of alteration in the collagen VII gene.
		Khavari and his group deduced that this collagen VII protein fragment might be necessary to allow cancer to spread.
	news-service.stanford.edu /news/2005/march30/med-cancer-033005.html (779 words)

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