Cellular metabolism · target hub

CPT1B

CPT1B (CPT1B)

CPT1B is a FAO / lipogenesis on the cellular metabolism axis. Validate function and tissue distribution with UniProt and primary literature. It is indexed under "Fatty acid oxidation (mitochondrial β-oxidation entry)" on our pathway page for antibodies, inhibitors, and assay guidance.

Back to pathway overviewSearch: CPT1BUniProt (Q9Y243)

Research notes

  • Combine with other genes in the same hub block via genetics or pharmacology to test non-redundant roles of CPT1B.
  • 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)
Enzyme activityCatalytic or substrate-channel changes
Steroid outputSteroid profile / metabolite readouts
Rare variantsSporadic variants—require validation

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

Assay readouts for CPT1B

  • Lipid metabolism: CPT1B with FAO or de novo lipogenesis tracing.
  • Etomoxir/C75/TOFA inhibitor controls.
  • Palmitate/BSA loading and lipid droplets.
  • Liver/adipose mouse models.

CPT1B 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 CPT1B studies (examples)

  • Tool lines: HepG2, 3T3-L1, Caco-2, HEK293T, MCF-7—screen by CPT1B expression and pathway context (CCLE/DepMap).
  • Combine with neighbors (CPT1A, CPT1C, CPT2, ACADVL) 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 CPT1B 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 CPT1B 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 CPT1B immunoprecipitation

  • Tagged overexpression: HEK293T FLAG/HA-CPT1B 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 CPT1B can differ in dosage, splicing, and compartmentation—in organoids/PDX, record passage, matrix, and drug history.

Quick search presets

CPT1BCPT1B antibodyCPT1B ligand/agonistmetabolism enzyme/transporter antibody

CPT1B-related antibodies (keyword-biased)

Adds CPT1B keyword bias atop the 细胞代谢 antibody pool—if sparse, use presets above or global search.

Neighboring targets (same hub)

CPT1ACPT1CCPT2ACADVLACADMHADHAHADHBEHHADH

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