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MAB1345

Sigma-Aldrich

Anti-Collagen Type VII Antibody, CT, clone LH7.2

ascites fluid, clone LH7.2, Chemicon®

Synonym(s):

Anti-EBD1, Anti-EBR1, Anti-NDNC8

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

mouse

Quality Level

100

antibody form

ascites fluid

antibody product type

primary antibodies

clone

LH7.2, monoclonal

species reactivity

human

manufacturer/tradename

Chemicon®

technique(s)

immunocytochemistry: suitable

isotype

IgG

NCBI accession no.

NM_000094.3

UniProt accession no.

Q02388

shipped in

dry ice

target post-translational modification

unmodified

Gene Information

human ... COL7A1(1294)

Specificity

Carboxy terminal peptide of type VII collagen.

Immunogen

Collagen type VII.

Application

Anti-Collagen Type VII Antibody, C-terminus, clone LH7.2 is an antibody against Collagen Type VII for use in IC.
Immunohistochemistry.

Optimal working dilutions must be determined by end user.

Physical form

Ascites. Liquid with 0.1% sodium azide.

Storage and Stability

Maintain at -20°C in convenient aliquots for up to 12 months. Avoid repeated freeze/thaw cycles.

Legal Information

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

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Storage Class Code

10 - Combustible liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Sabine E J Tanis et al.
Cell reports, 25(5), 1292-1303 (2018-11-01)
Epidermal homeostasis requires balanced progenitor cell proliferation and loss of differentiated cells from the epidermal surface. During this process, cells undergo major changes in their transcriptional programs to accommodate new cellular functions. We found that transcriptional and post-transcriptional mechanisms underlying
Distribution of basement membrane zone components in bullous lesions of subepidermal blistering diseases.
Satomi Hosoda et al.
The Journal of dermatology, 40(3), 211-212 (2013-01-09)
Dimitra Kiritsi et al.
The Journal of clinical investigation, 122(5), 1742-1746 (2012-04-03)
Spontaneous gene repair, also called revertant mosaicism, has been documented in several genetic disorders involving organs that undergo self-regeneration, including the skin. Genetic reversion may occur through different mechanisms, and in a single individual, the mutation can be repaired in
Wakana Matsumura et al.
The Journal of investigative dermatology, 139(10), 2115-2124 (2019-05-06)
Inherited skin disorders have been reported recently to have sporadic normal-looking areas, where a portion of the keratinocytes have recovered from causative gene mutations (revertant mosaicism). We observed a case of recessive dystrophic epidermolysis bullosa treated with cultured epidermal autografts
Cristina Chamorro et al.
Molecular therapy. Nucleic acids, 5(4), e307-e307 (2016-04-06)
Clonal gene therapy protocols based on the precise manipulation of epidermal stem cells require highly efficient gene-editing molecular tools. We have combined adeno-associated virus (AAV)-mediated delivery of donor template DNA with transcription activator-like nucleases (TALE) expressed by adenoviral vectors to
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