ATG16L1 Antibody [Janelia Fluor® 635]

Novus Biologicals, part of Bio-Techne | Catalog # NB110-82384JF635

Novus Biologicals, part of Bio-Techne
Catalog #
Availability
Size / Price
Qty
NB110-82384JF635
Print Quote
Bulk Order
Forumulation
Catalog #
BSA Free
NB110-82384
View Product
100% Guarantee

Key Product Details

Species Reactivity

Validated:

Human, Mouse

Applications

Immunoprecipitation, Western Blot

Label

Janelia Fluor 635

Antibody Source

Polyclonal Rabbit IgG

Concentration

Please see the vial label for concentration. If unlisted please contact technical services.

View all ATG16L1 Antibodies »

Product Summary for ATG16L1 Antibody [Janelia Fluor® 635]

Immunogen

A synthetic peptide within residues 1-100 of mouse ATG16L1. [Swiss-Prot# Q8C0J2]

Localization

Cytoplasm. Preautophagosomal structure, preautophagosomal structure membrane, peripheral membrane protein. Note: Localized to preautophagosomal structure (PAS) where it is involved in the membrane targeting of ATG5.

Clonality

Polyclonal

Host

Rabbit

Isotype

IgG

Applications for ATG16L1 Antibody [Janelia Fluor® 635]

Application
Recommended Usage

Immunoprecipitation

Optimal dilutions of this antibody should be experimentally determined.

Western Blot

Optimal dilutions of this antibody should be experimentally determined.
Application Notes
Optimal dilution of this antibody should be experimentally determined.
Please Note: Optimal dilutions of this antibody should be experimentally determined.

Formulation, Preparation, and Storage

Purification

Immunogen affinity purified

Formulation

50mM Sodium Borate

Preservative

0.05% Sodium Azide

Concentration

Please see the vial label for concentration. If unlisted please contact technical services.

Shipping

The product is shipped with polar packs. Upon receipt, store it immediately at the temperature recommended below.

Stability & Storage

Store at 4C in the dark.

Background: ATG16L1

Macroautophagy is the major inducible pathway for the general turnover of cytoplasmic constituents in eukaryotic cells, it is also responsible for the degradation of active cytoplasmic enzymes and organelles during nutrient starvation. Macroautophagy involves the formation of double-membrane bound autophagosomes which enclose the cytoplasmic constituent targeted for degradation in a membrane bound structure, which then fuse with the lysosome (or vacuole) releasing a single-membrane bound autophagic bodies which are then degraded within the lysosome (or vacuole). The APG12-APG5-APG16L complex is essential for the elongation of autophagic isolation membranes. This complex initially associates in uniform distribution with small vesicle membranes. During membrane elongation, the complex partitions, with a great concentration building on the outer side of the isolation membrane. Upon completion of the formation of the autophagosome, the APG12-APG5-APG16L dissociates from the membrane. There are 5 isoforms of this protein (in human), with theoretical molecular weights ranging from ~19-68 kDa.

Mutations in the ATG16L1 proitein have been associated with Crohn's disease.

Alternate Names

APG16 autophagy 16-like (S. cerevisiae), APG16L beta, APG16LFLJ10828, APG16-like 1, ATG16 autophagy related 16-like (S. cerevisiae), ATG16 autophagy related 16-like 1 (S. cerevisiae), ATG16A, ATG16L, autophagy-related protein 16-1, FLJ00045, FLJ10035, FLJ22677, IBD10, WD repeat domain 30, WDR30

Gene Symbol

ATG16L1

Additional ATG16L1 Products

Product Documents for ATG16L1 Antibody [Janelia Fluor® 635]

Product Datasheets

Certificate of Analysis

To download a Certificate of Analysis, please enter a lot number in the search box below.

Download SDS

Product Specific Notices for ATG16L1 Antibody [Janelia Fluor® 635]



Sold under license from the Howard Hughes Medical Institute, Janelia Research Campus.

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.

Privacy and Cookie Policy
Site Map
© Copyright 2024 Bio-Techne. All Rights Reserved.