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Merck
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SAB4200686

Sigma-Aldrich

Anti-Collagen, Type VII antibody, Mouse monoclonal

clone LH7.2, purified from hybridoma cell culture

Synonym(e):

Monoclonal Anti-Collagen, Type VII antibody produced in mouse, COL7A1, EBD1, EBDCT, EBR1, alpha 1, collagen, type VII

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About This Item

UNSPSC-Code:
12352203
NACRES:
NA.41

Biologische Quelle

mouse

Qualitätsniveau

200

Antikörperform

purified immunoglobulin

Antikörper-Produkttyp

primary antibodies

Klon

LH7.2, monoclonal

Form

buffered aqueous solution

Speziesreaktivität

human

Verpackung

antibody small pack of 25 μL

Konzentration

~1 mg/mL

Methode(n)

immunoblotting: suitable
immunohistochemistry: 1.5-3 μg/mL using frozen human tonsil sections

Isotyp

IgG1

Versandbedingung

dry ice

Lagertemp.

−20°C

Posttranslationale Modifikation Target

unmodified

Angaben zum Gen

human ... COL7A1(1294)

Verwandte Kategorien

Allgemeine Beschreibung

Monoclonal Anti-Collagen Type VII (mouse IgG1 isotype) is derived from the hybridoma LH7.2 produced by the fusion of mouse myeloma cells and splenocytes from BALB/c mice. Collagen Type VII (known also as Col7), which belongs to the collagen superfamily, is a major extracellular matrix component of the anchoring fibrils in lamina densa. COL7A1 (collagen type VII alpha 1 chain) gene codes for type VII collagen. It is located on human chromosome 3p. It is expressed by keratinocytes and fibroblasts. COL7A1 is the important component the anchoring fibrils.

Immunogen

insoluble fractions prepared from neonatal foreskin epidermal cells

Anwendung

Monoclonal Anti-Collagen, Type VII antibody produced in mouse has been used in:
  • enzyme-linked immunosorbent assay (ELISA)
  • immunoblotting
  • immunohistochemistry
  • immunofluorescence

Biochem./physiol. Wirkung

Collagen type VII is very essential for adhesive connection between the dermis and the epidermal basement membrane zone (BMZ). Mutations in collagen type VII cause dystrophic forms of epidermolysis bullosa (including recessive dystrophic epidermolysis bullosa (RDEB)), which manifest as skin fragility and malformed enamel.

Physikalische Form

Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.

Haftungsausschluss

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Lagerklassenschlüssel

12 - Non Combustible Liquids

WGK

nwg

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable

Analysenzertifikate (COA)

Suchen Sie nach Analysenzertifikate (COA), indem Sie die Lot-/Chargennummer des Produkts eingeben. Lot- und Chargennummern sind auf dem Produktetikett hinter den Wörtern ‘Lot’ oder ‘Batch’ (Lot oder Charge) zu finden.

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Die Dokumentenbibliothek aufrufen

Julia Niskanen et al.
PloS one, 12(5), e0177527-e0177527 (2017-05-12)
A rare hereditary mechanobullous disorder called epidermolysis bullosa (EB) causes blistering in the skin and the mucosal membranes. To date, nineteen EB-related genes have been discovered in human and other species. We describe here a novel EB variant in dogs.
Nonsense variant in COL7A1 causes recessive dystrophic epidermolysis bullosa in Central Asian Shepherd dogs
Niskanen J, et al.
PLoS ONE, 12(5), e0177527-e0177527 (2017)
Deletion of a Pathogenic Mutation-Containing Exon of COL7A1 Allows Clonal Gene Editing Correction of RDEB Patient Epidermal Stem Cells.
Mencia A, et al.
Molecular Therapy. Nucleic Acids, 11, 68-78 (2018)
Dystrophic epidermolysis bullosa: COL7A1 mutation landscape in a multi-ethnic cohort of 152 extended families with high degree of customary consanguineous marriages.
Vahidnezhad H, et al.
The Journal of Investigative Dermatology, 137(3), 660-669 (2017)
Genetic linkage of type VII collagen (COL7A1) to dominant dystrophic epidermolysis bullosa in families with abnormal anchoring fibrils.
Ryynaanen M, et al.
The Journal of Clinical Investigation (1992)

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