Activating Molecule In BECN1-Regulated Autophagy Protein 1 (AMBRA1) Antibody (ATTO390)

Product specifications

Primary Antibodies

Activating Molecule In BECN1-Regulated Autophagy Protein 1 (AMBRA1)

Rabbit

Human, Rat

WB: 1/1000, IF/ICC: 1/100. Optimal dilutions/concentrations should be determined by the end user.

Polyclonal

ATTO390

Peptide Affinity Purified

100 µg

WB, IF/ICC

PBS, 50% glycerol, 0.09% sodium azide.

Shipped within 5-12 working days.

Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles.

No

Q9C0C7

55626

NP_001254711.1

AMBRA1,DCAF3,DDB1 and CUL4-associated factor 3

Antibody anti-AMBRA1

RUO

Concentration: 1 mg/ml - 

Descripción

AMBRA1 or Activating Molecule in BECN1-regulated Autophagy Protein 1, is a key regulator of the autophagy process in mammalian cells. Autophagy is a cellular process involved in the degradation and recycling of damaged organelles, misfolded proteins, and other cellular components to maintain cellular homeostasis and respond to stress conditions. AMBRA1 was originally identified as a positive regulator of autophagy that interacts with Beclin 1 (encoded by the BECN1 gene), a core component of the class III phosphatidylinositol 3-kinase (PI3K) complex involved in autophagosome formation. Through its interactions with Beclin 1 and other autophagy-related proteins, AMBRA1 plays a crucial role in initiating and regulating the autophagy process.AMBRA1 interacts with Beclin 1 and helps to stabilize the Beclin 1 complex, promoting the nucleation of autophagosomal membranes and the initiation of autophagy. AMBRA1 regulates the size and maturation of autophagosomes, the double-membrane vesicles that sequester cargo for degradation during autophagy. It interacts with various proteins involved in autophagosome formation and fusion with lysosomes. AMBRA1 is also involved in crosstalk with signaling pathways that regulate autophagy, such as the mammalian target of rapamycin (mTOR) pathway and the p53 pathway. It can be phosphorylated and regulated by these pathways to modulate autophagy in response to cellular stress and nutrient availability.

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