Endocrine & hormone · target hub

IGFBP7

Insulin-like growth factor-binding protein 7 (IGFBP7)

IGFBP7 is a Hormone binding & transport on the endocrine & hormone axis. Binds IGF1 and IGF2 with a relatively low affinity. Stimulates prostacyclin (PGI2) production. Stimulates cell adhesion. Acts as a ligand for CD93 to play a role in angiogenesis (PubMed:38218180) It is indexed under "Lactation & GH-axis coupling" 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 IGFBP7.
  • 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 IGFBP7

  • Binding: IGFBP7 hormone SPR/radioligand binding.
  • Transport: membrane or nuclear transporter substrate uptake.
  • Binding globulins: free vs total hormone fractions.
  • Tissue distribution: liver/kidney expression & drug-interaction context.

IGFBP7 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 IGFBP7 studies (examples)

  • Tool lines: HepG2, HEK293T, MCF-7, HeLa, Caco-2—screen by IGFBP7 expression and pathway context (CCLE/DepMap).
  • Combine with neighbors (PRL, PRLR, GH1, GH2) 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 IGFBP7 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 IGFBP7 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 IGFBP7 immunoprecipitation

  • Tagged overexpression: HEK293T FLAG/HA-IGFBP7 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 IGFBP7 can differ in dosage, splicing, and compartmentation—in organoids/PDX, record passage, matrix, and drug history.

Quick search presets

IGFBP7-related antibodies (keyword-biased)

Adds IGFBP7 keyword bias atop the 内分泌和激素 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 endocrine & hormone hub for neighboring targets—cross-check PI3K, MAPK, RTK, and metabolism pages as needed.