PI3K/Akt/mTOR · target hub

ATG101

Autophagy-related protein 101 (ATG101)

ATG101 is a Autophagy/AMPK/DDR crosstalk with mTOR on the PI3K/Akt/mTOR axis. Autophagy factor required for autophagosome formation. Stabilizes ATG13, protecting it from proteasomal degradation It is indexed under "ULK complex (mTORC1-repressed autophagy initiation)" on our pathway page for antibodies, inhibitors, and assay guidance.

Research notes

  • Combine with other genes in the same hub block via genetics or pharmacology to test non-redundant roles of ATG101.
  • Annotate PIK3CA/PTEN and upstream RTK–Ras context when reading p-AKT, mTORC1/2, or lipid outputs.
  • Verify antibody clone, phospho-site, and stimulation; include KD/KO or inhibitor controls.

On the pathway hub (sections)

Genetic lesions & expression context (quick reference)

Type / exampleDomain / context (brief)
Expression contextTissue/cell-type–dependent expression
Rare variantsSporadic variants—require functional validation
Pathway couplingCo-occurs with neighboring nodes on the hub

Naming and prevalence vary by cohort and assay—annotate clinically with COSMIC, ClinVar, OncoKB, and datasheets; research context only.

Assay readouts for ATG101

  • Autophagy: LC3-II, p62, ULK1 complex phospho-status under mTORC1 restraint.
  • AMPK: p-ACC, p-TSC2 in energy-stress contexts.
  • DDR: γH2AX, CHK1/2 phosphorylation in damage models.
  • Pair with Akt/mTOR inhibitors to map parallel survival programs.

ATG101 experimental notes

Examples below reflect common literature and public resources (e.g., CCLE, DepMap)—validate genotypes, expression, and passage in your own stocks before committing assays.

[1] Cell lines commonly used for ATG101 studies (examples)

  • Tool lines: U2OS, MEFs, HEK293T, HCT116, A549—screen by ATG101 expression and pathway context (CCLE/DepMap).
  • Combine with neighbors (ULK1, ULK2, ATG13, RB1CC1) via KD/pharmacology to test non-redundancy.
  • Overexpression/rescue in HEK293T supports mechanism and IP workflows.
  • Isogenic/CRISPR models separate pathway dependency from bypass survival.

[2] Cell samples for ATG101 Western blot

  • Whole-cell lysates—optimize RIPA/NP-40 per antibody; phosphatase inhibitors for phospho blots.
  • Stimulation: serum starvation ± insulin/EGF or amino-acid withdrawal/refeed as relevant.
  • Controls: siRNA/shRNA, CRISPR KO, or inhibitors to validate band specificity.
  • Loading: BCA normalization; subcellular fractionation when needed.

[3] Tissue samples for ATG101 Western blot

  • Matched tumor/adjacent frozen tissues after pathology review.
  • Mouse GEMM or xenografts—mind species antibody cross-reactivity.
  • Primary cells/PDCs when ethically approved.
  • FFPE needs specialized extraction; frozen tissue preferred for phospho work.

[4] Cell samples for ATG101 immunoprecipitation

  • Tagged overexpression: HEK293T FLAG/HA-ATG101 for complex capture.
  • Endogenous IP: high-expression lines; often ≥1–5×10⁶ cells per IP.
  • Stimulation: ligand or nutrient treatments enrich interactions—pilot time courses.
  • Controls: isotype IgG, empty vector, KD/KO negatives.

Human tissues and primary cells require ethics/IRB approval; tumors are heterogeneous—record histotype, site, and preservation conditions.

Bypass & related pathways

Models & genetics note

Overexpression vs endogenous ATG101 can differ in dosage, splicing, and compartmentation—in organoids/PDX, record passage, matrix, and drug history.

Quick search presets

ATG101-related antibodies (keyword-biased)

Adds ATG101 keyword bias atop the PI3K/Akt/mTOR antibody pool—if sparse, use presets above or global search.

FAQ

This content supports research reagents and pathway education—not medical advice. Annotate mutations, drug indications, and protocols with authoritative databases, datasheets, and institutional oversight.

Last reviewed: 2026-05-18

Related on this site

See the PI3K/Akt/mTOR hub for neighboring nodes and assay guidance—cross-check MAPK, RTK, metabolism, and autophagy pages as needed.