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Anti-ATG9 [Atg9 14F2 8B1]
RECENTLY UPDATED

Invented by Dr Sharon Tooze at Cancer Research UK London Research Institute: Lincoln's Inn Fields

Info

Catalogue Number 151525
Applications
RECENTLY UPDATED
ELISA IHC IF IP WB
Antigen/Gene or Protein Targets Autophagy-related protein 9 (ATG9)
Reactivity Human, Mouse and Rat
Relevance Autophagy is an important process associated with infectious disease, neurodegeneration, cancer and the maintenance of cellular homeostasis. ATG9 is an essential component of the autophagy machinery and is found on autophagosomes. It is a multi-spanning membrane protein which makes it useful for sub-cellular localization studies. The detection of this protein provides important information about cell health and survival.
Host Hamster
Immunogen Conserved C-terminal synthetic peptide of Human ATG9 sequence
Positive Control Endogenous protein, tagged over expressed protein and sRNA-depleted HEK 293 cells,
Subclass IgG
Molecular Weight (kDa) 105
Myeloma Used P3X63Ag8.653
Recommended Growing Conditions Hybridoma Serum Free Medium + 7.5% FBS + 10 µg/ml gentamycin
Strain Armenian
Research Area Cancer, Cardiovascular, Cell Signaling & Signal Transduction, Metabolism, Neurobiology, Protein Degradation

References

There are 4 reference entries for this reagent.

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References: 4 entries
RECENTLY UPDATED

ATG9A shapes the forming autophagosome through Arfaptin 2 and phosphatidylinositol 4-kinase IIIβ

IHC IP

Chan et al. 2009. Mol Cell Biol. 29(1):157-71. PMID: 18936157.

Kinase-inactivated ULK proteins inhibit autophagy via their conserved C-terminal domains using an Atg13-independent mechanism.

Europe PMC ID: 18936157

Starvation and ULK1-dependent cycling of mammalian Atg9 between the TGN and endosomes.

IHC IP


Add a reference

References: 4 entries
RECENTLY UPDATED

ATG9A shapes the forming autophagosome through Arfaptin 2 and phosphatidylinositol 4-kinase IIIβ

IHC IP

Chan et al. 2009. Mol Cell Biol. 29(1):157-71. PMID: 18936157.

Kinase-inactivated ULK proteins inhibit autophagy via their conserved C-terminal domains using an Atg13-independent mechanism.

Starvation and ULK1-dependent cycling of mammalian Atg9 between the TGN and endosomes.

IHC IP


Add a reference