Cellular metabolism · target hub

EGLN1

EGLN1 (EGLN1)

EGLN1 is a AMPK / mTOR / HIF on the cellular metabolism axis. Validate function and tissue distribution with UniProt and primary literature. It is indexed under "mTORC1/2 & HIF axis" on our pathway page for antibodies, inhibitors, and assay guidance.

Back to pathway overviewSearch: EGLN1UniProt (Q9Y243)

Research notes

  • Combine with other genes in the same hub block via genetics or pharmacology to test non-redundant roles of EGLN1.
  • 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 EGLN1

  • Nutrient sensing: EGLN1 with p-AMPK, p-S6K, or HIF targets.
  • Amino-acid/glucose starvation and mTOR inhibitors.
  • Normoxia vs hypoxia (1% O2).
  • VHL/EGLN genetic backgrounds.

EGLN1 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 EGLN1 studies (examples)

  • Tool lines: HeLa, HEK293T, MCF-7, U87, MIN6—screen by EGLN1 expression and pathway context (CCLE/DepMap).
  • Combine with neighbors (MTOR, RPTOR, RICTOR, MLST8) 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 EGLN1 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 EGLN1 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 EGLN1 immunoprecipitation

  • Tagged overexpression: HEK293T FLAG/HA-EGLN1 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 EGLN1 can differ in dosage, splicing, and compartmentation—in organoids/PDX, record passage, matrix, and drug history.

Quick search presets

EGLN1EGLN1 antibodyEGLN1 ligand/agonistmetabolism enzyme/transporter antibody

EGLN1-related antibodies (keyword-biased)

Adds EGLN1 keyword bias atop the 细胞代谢 antibody pool—if sparse, use presets above or global search.

Neighboring targets (same hub)

MTORRPTORRICTORMLST8AKT1AKT2TSC1TSC2

External databases & resources

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.

Cellular metabolism·PI3K/Akt/mTOR·MAPK/ERK·Receptor tyrosine kinase·Transmembrane transport