Endocrine & hormone · target hub

LEPR

Leptin receptor (LEPR)

LEPR is a Metabolic / incretin hormones on the endocrine & hormone axis. Receptor for hormone LEP/leptin (Probable) (PubMed:22405007). On ligand binding, mediates LEP central and peripheral effects through the activation of different signaling pathways such as JAK2/STAT3 and MAPK cascade/FOS. In the hypothalamus, LEP acts as an appetite-regulating fac… It is indexed under "Adipokines & energy-sensing endocrine crosstalk" on our pathway page for antibodies, inhibitors, and assay guidance.

Back to pathway overviewSearch: LEPRUniProt (P48357)

Research notes

  • Combine with other genes in the same hub block via genetics or pharmacology to test non-redundant roles of LEPR.
  • For nuclear receptors pair ligands, co-regulators, and reporter assays; for membrane receptors note GPCR/RTK downstream and desensitization.
  • 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 LEPR

  • Islet/liver: LEPR with insulin secretion, gluconeogenesis, or lipid readouts.
  • Incretins: GLP-1/GIP stimulation and receptor agonists.
  • p-AKT / p-ERK: combined nutrient and hormone stimulation.
  • Metabolic disease models: tissue insulin sensitivity.

LEPR 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 LEPR studies (examples)

  • Tool lines: MIN6, INS-1, HepG2, 3T3-L1, HEK293T—screen by LEPR expression and pathway context (CCLE/DepMap).
  • Combine with neighbors (LEP, ADIPOQ, ADIPOR1, ADIPOR2) 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 LEPR 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 LEPR 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 LEPR immunoprecipitation

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

Quick search presets

LEPRLEPR antibodyLEPR ligand/agonisthormone/receptor antibody

LEPR-related antibodies (keyword-biased)

Adds LEPR keyword bias atop the 内分泌和激素 antibody pool—if sparse, use presets above or global search.

Neighboring targets (same hub)

LEPADIPOQADIPOR1ADIPOR2RETNRBP4NAMPTFGF21

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 endocrine & hormone hub for neighboring targets—cross-check PI3K, MAPK, RTK, and metabolism pages as needed.

Endocrine & hormone·PI3K/Akt/mTOR·MAPK/ERK·Receptor tyrosine kinase·Metabolism