Endocrine & hormone · target hub

NR1I3

Nuclear receptor subfamily 1 group I member 3 (NR1I3)

NR1I3 is a Nuclear receptor / transcriptional control on the endocrine & hormone axis. Binds and transactivates the retinoic acid response elements that control expression of the retinoic acid receptor beta 2 and alcohol dehydrogenase 3 genes. Transactivates both the phenobarbital responsive element module of the human CYP2B6 gene and the CYP3A4 xenobiotic response… It is indexed under "Nuclear receptor superfamily (major members)" on our pathway page for antibodies, inhibitors, and assay guidance.

Back to pathway overviewSearch: NR1I3UniProt (Q14994)

Research notes

  • Combine with other genes in the same hub block via genetics or pharmacology to test non-redundant roles of NR1I3.
  • 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)
LBD / AF2Ligand-binding or AF2 domain variants
HotspotHormone-dependent tumor hotspots (gene-specific)
Cofactor switchingAltered co-regulator recruitment

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

Assay readouts for NR1I3

  • Reporter / ChIP: NR1I3 promoter-luciferase or ChIP-qPCR.
  • Ligand treatments: estrogen/androgen/progesterone/glucocorticoid as appropriate.
  • Co-regulators: SRC/p300 co-activator or co-repressor co-IP.
  • Tumor specimens: receptor IHC with mutation/amplification annotation.

NR1I3 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 NR1I3 studies (examples)

  • Tool lines: MCF-7, T47D, LNCaP, MDA-MB-231, HEK293T—screen by NR1I3 expression and pathway context (CCLE/DepMap).
  • Combine with neighbors (NR0B1, NR0B2, THRA, THRB) 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 NR1I3 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 NR1I3 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 NR1I3 immunoprecipitation

  • Tagged overexpression: HEK293T FLAG/HA-NR1I3 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 NR1I3 can differ in dosage, splicing, and compartmentation—in organoids/PDX, record passage, matrix, and drug history.

Quick search presets

NR1I3NR1I3 antibodyNR1I3 ligand/agonisthormone/receptor antibody

NR1I3-related antibodies (keyword-biased)

Adds NR1I3 keyword bias atop the 内分泌和激素 antibody pool—if sparse, use presets above or global search.

Neighboring targets (same hub)

NR0B1NR0B2THRATHRBRARARARBRARGRXRA

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