ATG9A Antibody

Product Specifications

Background

ATG9A Antibody: Autophagy, the process of bulk degradation of cellular proteins through an autophagosomic-lysosomal pathway is important for normal growth control and may be defective in tumor cells. It is involved in the preservation of cellular nutrients under starvation conditions as well as the normal turnover of cytosolic components. This process is negatively regulated by TOR (Target of rapamycin) through phosphorylation of autophagy protein APG1. ATG9A, a multi-spanning membrane protein localizing to the Golgi apparatus and late endosomes, has been proposed to mediate membrane transport to generate autophagosomes. ATG9A has also been implicated as a regulator of STING (stimulator of interferon genes) -mediated innate immune response.

NCBI Gene ID

79065

Swiss Prot

Q7Z3C6

Accession Number

NP_076990

Host

Rabbit

Reactivity

Human, Mouse, Rat

Clonality

Polyclonal

Conjugation

Unconjugated

Type

Primary Antibodies

Field of Research

Autophagy

Purification

ATG9A Antibody is affinity chromatography purified via peptide column.

Positive Control

Cat. No. 1401 - Mouse Heart Tissue Lysate

Concentration

1 mg/mL

Homology

Predicted species reactivity based on immunogen sequence: Bovine: (94%)

Buffer

ATG9A Antibody is supplied in PBS containing 0.02% sodium azide.

Modification

None

Shipping Conditions

Blue Ice

Storage Conditions

ATG9A antibody can be stored at 4˚ C for three months and -20˚ C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.

Fragment

IgG

Symbol

ATG9A

Positive Control 2

Cat. No. 10-501 - Human Heart Tissue Slide

NCBI Official Name

ATG9 autophagy related 9 homolog A (S. cerevisiae)

NCBI Organism

Homo sapiens

Background Reference 01

Gozuacik D and Kimchi A. Autophagy as a cell death and tumor suppressor mechanism. Oncogene2004; 23:2891-906.

Background Reference 02

Kisen GO, Tessitore L, Costelli P, et al. Reduced autophagic activity in primary rat hepatocellular carcinoma and ascites hepatoma cells. Carcinogenesis1993; 14:2501-5.