Promotional price valid on web orders only. Your contract pricing may differ. Interested in signing up for a dedicated account number?
Learn More

ATG16L1 Mouse anti-Human, Clone:8F8C2, Abnova™

Mouse monoclonal antibody raised against recombinant human ATG16L1.

Supplier:  Abnova Corporation MAB17120

Catalog No. 89-333-462


Only null left
Add to Cart

Description

Description

Autophagy is the major intracellular degradation system delivering cytoplasmic components to lysosomes, and it accounts for degradation of most long-lived proteins and some organelles. Cytoplasmic constituents, including organelles, are sequestered into double-membraned autophagosomes, which subsequently fuse with lysosomes. ATG16L1 is a component of a large protein complex essential for autophagy (Mizushima et al., 2003 [PubMed 12665549]).[supplied by OMIM]
Specifications

Specifications

ATG16L1
Monoclonal
Unconjugated
ELISA (1:10000)
Western Blot (1:500-1:2000)
Immunohistochemistry
Immunocytochemistry
Flow Cytometry
The optimal working dilution should be determined by the end user.
ATG16L1
Mouse
100 μg
Human
Antibody
IgG1
ELISA, Western Blot
8F8C2
ATG16 autophagy related 16-like 1 (S. cerevisiae)
In PBS (0.05% sodium azide)
APG16L, ATG16L, FLJ00045, FLJ10035, FLJ10828, FLJ22677, IBD10, WDR30
Recombinant protein corresponding to amino acid 11-257 of human ATG16L1 from E. coli.
55054
Store at 4°C. For long term storage store at -20°C.
Aliquot to avoid repeated freezing and thawing.
Liquid
Product Suggestions

Product Suggestions

Videos
SDS
Documents

Documents

Product Certifications
Promotions

Promotions

Product Content Correction

Your input is important to us. Please complete this form to provide feedback related to the content on this product.

Product Title

By clicking Submit, you acknowledge that you may be contacted by Fisher Scientific in regards to the feedback you have provided in this form. We will not share your information for any other purposes. All contact information provided shall also be maintained in accordance with our Privacy Policy.

Your feedback has been submitted: Thank you for helping us improve our website.