Cellular metabolism · target hub

ATP5F1C

ATP5F1C (ATP5F1C)

ATP5F1C is a OXPHOS / pentose phosphate on the cellular metabolism axis. Validate function and tissue distribution with UniProt and primary literature. It is indexed under "OXPHOS (ETC / ATP synthase representatives)" 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 ATP5F1C.
  • Pair metabolic flux with 13C tracing, Seahorse OCR/ECAR, or metabolomics; nutrient withdrawal/refeed controls.
  • Verify antibody clone, compartment, 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 ATP5F1C

  • OXPHOS/PPP: ATP5F1C with OCR, ATP, or NADPH readouts.
  • Oligomycin/antimycin A/rotenone pharmacology.
  • Oxidative stress and GSH/GSSG.
  • One-carbon/folate LC-MS for PPP nodes.

ATP5F1C 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 ATP5F1C studies (examples)

  • Tool lines: HeLa, HepG2, Jurkat, HEK293T, A549—screen by ATP5F1C expression and pathway context (CCLE/DepMap).
  • Combine with neighbors (NDUFS1, NDUFS3, UQCRC2, CYCS) 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 ATP5F1C 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 ATP5F1C 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 ATP5F1C immunoprecipitation

  • Tagged overexpression: HEK293T FLAG/HA-ATP5F1C 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 ATP5F1C can differ in dosage, splicing, and compartmentation—in organoids/PDX, record passage, matrix, and drug history.

Quick search presets

ATP5F1C-related antibodies (keyword-biased)

Adds ATP5F1C keyword bias atop the 细胞代谢 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 cellular metabolism hub for neighboring targets—cross-check PI3K, MAPK, and transmembrane transport pages as needed.