Cellular metabolism · target hub

SLC7A11

SLC7A11 (SLC7A11)

SLC7A11 is a Glutamine metabolism / transport on the cellular metabolism axis. Validate function and tissue distribution with UniProt and primary literature. It is indexed under "SLCs: glucose, lactate, amino acids (representative)" 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 SLC7A11.
  • 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)
Ligand stimulationLigand-dependent phosphorylation
GPCR desensitizationβ-arrestin / internalization control
CN / expressionCopy number & tissue expression

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

Assay readouts for SLC7A11

  • Glutamine axis: SLC7A11 with 13C-glutamine anaplerosis and transport.
  • CB-839 / BPTES where relevant.
  • SLC substrate competition assays.
  • Hypoxia plus nutrient stress.

SLC7A11 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 SLC7A11 studies (examples)

  • Tool lines: HeLa, A549, MCF-7, HEK293T, HepG2—screen by SLC7A11 expression and pathway context (CCLE/DepMap).
  • Combine with neighbors (SLC2A1, SLC16A1, SLC16A3, SLC16A7) 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 SLC7A11 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 SLC7A11 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 SLC7A11 immunoprecipitation

  • Tagged overexpression: HEK293T FLAG/HA-SLC7A11 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 SLC7A11 can differ in dosage, splicing, and compartmentation—in organoids/PDX, record passage, matrix, and drug history.

Quick search presets

SLC7A11-related antibodies (keyword-biased)

Adds SLC7A11 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.