MAB1345
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
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biological source
mouse
Quality Level
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.
UniProt accession no.
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.
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
recommended
Product No.
Description
Pricing
wgk_germany
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
Certificates of Analysis (COA)
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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
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
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)
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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