Purified anti-ATG7 Antibody, ATG7, A17129A,BioLegend,625851

Host

Mouse

Reactivity

Human, Mouse, Rat

Application

WB - Quality testedICC, IHC-P, KO/KD-WB - Verified

Platform ID

BAB800017860

BioLegend

Headquarters

8999 BioLegend Way San Diego, CA 92121 United States

Contact

Tel: 1-858-455-9588
Fax: +49 (4131) 7023913

Email:

Product Specifications
Scientific Background

Specifications

NamePurified anti-ATG7 Antibody, ATG7, A17129A
Cat. No.625851
HostMouse
RRIDAB_3083415 (BioLegend Cat. No. 625851)AB_3083415 (BioLegend Cat. No. 625852)
IsotypeMouse IgG2b, κ
ReactivityHuman, Mouse, Rat
ApplicationWB - Quality testedICC, IHC-P, KO/KD-WB - Verified
ClonalityMonoclonal
Clone NumberA17129A
Concentration0.5 mg/mL
TargetATG7
ImmunogenRecombinant fragment of human ATG7
PurityThe antibody was purified by affinity chromatography.
FormulationPhosphate-buffered solution, pH 7.2, containing 0.09% sodium azide
StorageThe antibody solution should be stored undiluted between 2°C and 8°C.
Regulatory StatusResearch Use Only

Scientific Background

ATG7 is an E1-like ligase that plays a central role in autophagosome biogenesis by conjugating ATG5 to ATG12 which degrades and recycles damaged organelles, protein aggregates, and invading pathogens. ATG7 interacts with other ATG proteins, such as ATG3, ATG10, and ATG16L1, to form a complex that is required for autophagy, also regulates immunity, cell death, and protein secretion, and independently regulates the cell cycle and apoptosis. It also participates in lipidation of the ATG8 protein, which is essential for autophagosome formation. Additionally, ATG7 has been shown to interact with other proteins outside of the autophagy pathway, such as p53, to regulate apoptosis. Disrupting ATG7-dependent autophagy has been shown to cause electromotility disturbances, outer hair cell loss, and deafness in mice. ATG7 dysfunction has been associated with various human diseases, including cancer, neurodegeneration, and infection. ATG7 dysfunction and disease was found in patients with biallelic ATG7 variants and childhood-onset neuropathology. Furthermore, ATG7 has been shown to induce basal autophagy and rescue autophagic deficiency in CryABR120Gcardiomyocytes.

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