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A7356

Sigma-Aldrich

Anti-Atg16L antibody produced in rabbit

fractionated antiserum, buffered aqueous solution

Synonym(s):

Anti-APG16L, Anti-ATG16 autophagy related 16-like 1 (S. cerevisiae), Anti-ATG16L1

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

200

conjugate

unconjugated

antibody form

fractionated antiserum

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen ~70 kDa (several isonform bands)

species reactivity

rat, mouse, human

technique(s)

western blot: 1:500-1:1,000 using whole extracts of human A549 cells, rat PC12 cells, and HEK-293T cells expressing mouse Atg16l

UniProt accession no.

Q676U5

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... ATG16L1(55054)
mouse ... Atg16l1(77040)
rat ... Atg16l1(363278)

General description

ATG16L is a component of a large protein complex that is critical for autophagy.
Autophagy-related 16-like 1 (ATG16L1) is an autophagy gene, that is expressed in the colon, small intestine, intestinal epithelial cells, leukocytes and spleen. Atg16L is expressed in different isoform patterns depending on the tissue.

Immunogen

synthetic peptide correspopnding to amino acids 2-15 of mouse Atg16l, conjugated to KLH via a C-terminal cysteine residue. The corresponding sequence is identical in rat and human.

Application

Anti-Atg16L antibody produced in rabbit has been used in western blotting.

Biochem/physiol Actions

Atg16L is involved in LC3 lipidation during the formation of autphagosomes. Studies have reported that Atg16L may also function as a mammalian Rab33 effector.
Autophagy-related 16-like 1 (ATG16L1) modulates host immune responses and is linked with several diseases, like cardiovascular disease (CVD). Atg16 multimeric complex plays an essential role in autophagy. Atg16L interacts with both Atg5 and additional Atg16L monomers. Together with Atg12-Atg5 conjugate, Atg16L associates with the autophagic isolation membrane for the duration of autophagosome formation.

Physical form

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

Disclaimer

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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Storage Class Code

10 - Combustible liquids

WGK

WGK 2

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Personal Protective Equipment

dust mask type N95 (US), Eyeshields, Gloves

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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Mitsunori Fukuda et al.
Autophagy, 4(6), 824-826 (2008-08-02)
Atg16L is a factor that is essential for elongation of the isolation membrane (also called phagophore), a precursor of the autophagosome. Atg16L facilitates LC3/Atg8-conjugation to phosphatidylethanolamine by forming an oligomeric complex with Atg12-conjugated Atg5 and recruiting an LC3-Atg3 intermediate to
Arin K Oestreich et al.
Endocrinology, 161(1) (2019-12-27)
Uterine receptivity is critical for establishing and maintaining pregnancy. For the endometrium to become receptive, stromal cells must differentiate into decidual cells capable of secreting factors necessary for embryo survival and placental development. Although there are multiple reports of autophagy
Vanessa M Hubbard-Lucey et al.
Immunity, 41(4), 579-591 (2014-10-14)
Atg16L1 mediates the cellular degradative process of autophagy and is considered a critical regulator of inflammation based on its genetic association with inflammatory bowel disease. Here we find that Atg16L1 deficiency leads to an exacerbated graft-versus-host disease (GVHD) in a
Ferritinophagy drives uropathogenic Escherichia coli persistence in bladder epithelial cells
Bauckman KA and Mysorekar IU
Autophagy, 12(5), 850-863 (2016)
Bin Cao et al.
JCI insight, 1(21), e86654-e86654 (2016-12-27)
The placenta is a barrier against maternal-fetal transmission of pathogens. Placental infections can cause several adverse pregnancy outcomes, including preterm birth (PTB). Yet, we have limited knowledge regarding the mechanisms the placenta uses to control infections. Here, we show that
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