ATG9A Antibodies

Autophagy-related protein 9A (ATG9A)

Involved in autophagy and cytoplasm to vacuole transport (Cvt) vesicle formation. Plays a crucial role in the business of this preautophagosomal structure/phagophore assembly site (PAS), the nucleating site for formation of the sequestering vesicle.

Cycles between a juxta-nuclear trans-Golgi network compartment and late endosomes. Nutrient starvation induces accumulation on autophagosomes.

Gene Information

Human
Gene Name:	ATG9A
Uniprot:	Q7Z3C6
Entrez:	79065

Family

Belongs to:
ATG9 family

Alternative Names

APG9 autophagy 9-like 1 (S. cerevisiae); APG9 autophagy 9-like 1; APG9L1APG9-like 1; ATG9 autophagy related 9 homolog A (S. cerevisiae); autophagy 9-like 1 protein; autophagy-related protein 9A; FLJ22169; mATG9; MGD3208

Molecular Weight

Mass (kDA):
94.447 kDA

Genomic Context

Human
Location:	2q35
Sequence:	2; NC_000002.12 (219219380..219229636, complement)

Subcellular Localizations

Cytoplasmic vesicle, autophagosome membrane; Multi-pass membrane protein. Golgi apparatus, trans-Golgi network membrane; Multi-pass membrane protein. Late endosome membrane; Multi-pass membrane protein. Endoplasmic reticulum membrane; Multi-pass membrane protein. Under amino acid starvation or rapamycin treatment, redistributes from a juxtanuclear clustered pool to a dispersed peripheral cytosolic pool. The starvation-induced redistribution depends on ULK1, ATG13, as well as SH3GLB1.

Diseases

• Sting Injury
• Innate Immune Response
• Malignant Squamous Cell Neoplasm
• Infection By Cryptococcus Neoformans
• Ataxia
• Carcinoma
• Endoplasmic Reticulum Stress
• Meningoencephalitis
• Ataxia Telangiectasia
• Malignant Neoplasms

• Neoplasms
• Nervousness
• Telangiectasis
• Salmonella Infections

Interacting Proteins

• KRT31
• KRTAP10-8
• KRTAP4-2
• KRTAP5-9
• LONRF1

• NOTCH2NL
• REL
• TBK1

Pathways

• Autophagy
• Cell Death
• Innate Immune Response
• Immune Response
• Transport
• Phagocytosis
• Autophagic Cell Death
• Vesicle-mediated Transport
• Catabolic Process

• Pathogenesis
• Rna Interference
• Localization

PTMs

• Phosphorylation

• Acetylation

Research Areas

• Autophagy
• Cancer
• Cell Biology
• Neurodegeneration
• Neuroscience

• Tumor Suppressors
• Ubiquitin Proteasome Pathway

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/ATG9A

Boster Bio: Best Uses Of The Autophagy Marker

The Boster Bio: Best uses of the Autophagy Marker antibody is a powerful tool that allows researchers to identify genes which promote autophagy. These genes can be used for a variety of biological experiments and applications. The antibody is highly specific for ATG9A tyrosinekinase. Boster Bio will accept research results and provide samples and product credits. This service is open to all scientists, regardless of their field or discipline.

Boster's primary antibodies of high-affinity are highly specific

Boster Bio offers over 16,000 ELISA kits and other products for research. Each product has been thoroughly tested for ELISA and WB applications. Boster has rabbit polyclonal and mouse primary and second antibodies. Boster products come with a Boster Quality Warranty for optimal results.

The ATG9A marker is used in several different flow cytometry applications. Flowcytometry is a powerful technique, with many applications in biomedical and scientific research. Using antibodies to count and detect a wide variety cells and particles, flow cytometry is a technique. These antibodies can be monoclonal (or polyclonal) and have a strong track record of success. High-affinity primary antibodies from the company are frequently cited and continue being useful to researchers around the world.

The company makes monoclonal and multiclonal antibodies as well as diagnostic kits. Brighter Ideas specializes on anti-GFP polyclonal antibody production using high-purity native Aequoria victoria GFP proteins. It also sponsors an online course in protein purification. Calbiochem offers a large variety of primary antibodies, secondary antibodies, and accessory products.

Two antigens can be simultaneously visualized or sequentially in this technique. To ensure that the primary or secondary antibodies do NOT cross-react with each other, the pigments used to visualize one must not block the view of the other. Using optical filter combinations, multiple primary-secondary antibody pairs can be visualized in a single image. Researchers can identify up to 61 different antibodies on the same tissue.

Research can be aided by high-affinity primary antibodies. However, they can also pose problems. High affinity can make it difficult to separate antigens from antibodies, and may require harsher methods for column elution. Furthermore, high affinity means the antibody may be difficult to purify, which can result in denaturation. These antibodies may not be the best for clinical use.

Alper Biotech is another manufacturer of monoclonal antibody. Alper Biotech produces highly sensitive and specific antibodies. It also sells antibodies for rapid diagnostic tests. Over 5000 polyclonal antibody stock is also available at the company. Alpha Diagnostic International sells monoclonal antibodies, custom peptides, and neurobiological antigens. This list isn't exhaustive and you can find many antibodies for your research applications on their site.

Autophagy induction detection

ATG9A's role in autophagy is assessed by the detection of autophagy-inducible protein. It is essential for normal autophagy progression because it tethers membranes Atg9 positive at PAS to form an phagophore. TRAPPIII, a protein responsible for controlling ATG9's activity, promotes its trafficking and maintains the ATG9 Pool during starvation.

ATG9 is essential for autophagy, but the lack of it inhibits both starvation-induced and developmental autophagy. We used null mutants that were newly created to examine the role played by Atg9 in autophagy. We stained cells expressing Atg9 with the pH-sensitive fluorescent dye LysoTracker (which has long been used to detect acidic lysosomes). Atg9-deficient autophagy promoting proteins did not show punctate staining when exposed to nutrients.

When autophagy-inducing proteins are ablated, mice display distal axonal swellings. It is also possible to see ER accumulation in the atg5 null mouse axons. HSP cases comprise 60% of cases due to a deficit in factors that are critical for ER metabolism. ATL1-dependent remodeling is necessary for selective inclusion of ER in autophagosomes.

The ATG9A ATG9A protein, which is the only mammalian Transmembrane ATG-protein, relies on vesicular sorts to distribute itself. It plays a key role in autophagosome maturation. ATG9A sorting is essential for maintaining autophagosomes at the distal end axons. Moreover, atg9a deficiency in mice has been associated with dysgenesis of the corpus callosum.

Interestingly, atg9 also causes a decrease the level of TSC2, which can be a crucial signal for TOR signals. This suggests that Atg9 may function as a negative feedback loop, which regulates autophagy by inhibiting TOR signaling. In addition to autophagy inducing genes, it also affects cell growth and tissue homeostasis.

We were able visualize the movement of autophagosomes within a cultured DIV-4 Cell line by using a Kaleidoscope and a Kymograph. These images are displayed at high magnification and a scale of 2 mm. The RFP-LC3 tracks represent the accumulation of ER and incorporation of it into the double membraned autophagosome. The resulting kymographs were then used to calculate the overall motion of autophagosomes.

Atg9 deletion causes abnormal posterior midgut enlargement and increased proliferation. Atg9-mutant intestinal tissue shows similar ratios of Pros+ cells and Delta+ cells. This suggests that Atg9 may not be essential for the regulation ISC growth under normal conditions. This study has important implications for the development of a new therapy for digestive disorders.

We found a genetically-modified ATG9A knockout mouse that showed an ap4e1 dependent increase in ATG9 handling. AP4E1 co-immunoprecipitates with ATG9A and interacts with it. Western blotting of ATG9A showed an increase in protein levels among KO mice. We also found increased levels of protein in KO mice when ATG9A and AP4E1 knockout were co-injected into the embryos of nanos-Cas9-expressing flies.

AMPK-Ulk1/2 regulates autophagy

AMPK, a protein kinase, interacts with ULK1, the autophagy initiator. Until recently it was believed that AMPK controlled mTOR and autophagy. New research shows that ULK1 as well as AMPK regulate autophagy via two distinct pathways. The first is by activating ULK1 and the second is by phosphorylating ULK1 via AMPK.

AMPK regulates the Vps34 protein complex. However, it also acts downstream as a regulator for mTOR1 or Ulk1, which are essential for autophagy. These two proteins play a discordant function in autophagy in mammals because they are required for different signaling events. The function of Ulk1 and Ulk2 is not yet understood.

The AMPK/ULK1/2 pathway promotes AMPK-ULK1/2 by regulating the activity regulators of mitochondrial metabolism, including ULK1. This pathway is associated with glyceraldehyde-3-phosphate dehydrogenase and ACC. ULK1 & ULK2 also get phosphorylated through the AMPK kinase Akt.

Ulk1 promotes Atg13 transfer to mitochondria in damaged tissues. ULK1-induced phosphorylation FUNDC1 improves its interaction and interaction with LC3. Mitophagy, which is required for cell homeostasis and neurodegeneration, can be impaired by ULK1-induced phosphorylation of FUNDC1. This is vital for maintaining mitochondrial quality.

ULK1 activates when the body has run out of energy. AMPK blocks mTOR activity when there is high energy. Moreover, mTOR activates ULK1 and inhibits autophagy. In absence of mTOR activity ULK1 is not able to interact with mTOR to promote autophagy.