Cellular metabolism · target hub

PDK2

PDK2 (PDK2)

PDK2 is a Glycolysis / glucose uptake on the cellular metabolism axis. Validate function and tissue distribution with UniProt and primary literature. It is indexed under "Core glycolytic enzymes (flux & branching)" 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 PDK2.
  • 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 PDK2

  • Glycolytic flux: PDK2 activity, 13C-glucose tracing, or Seahorse ECAR.
  • Glucose withdrawal/refeed; 2-DG or HK/PK inhibitor controls.
  • Lactate/pyruvate ratio and medium pH.
  • Tumor vs normal expression (TCGA/proteomics).

PDK2 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 PDK2 studies (examples)

  • Tool lines: HeLa, HepG2, MCF-7, HEK293T, A549—screen by PDK2 expression and pathway context (CCLE/DepMap).
  • Combine with neighbors (TPI1, GAPDH, PGK1, PGAM1) 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 PDK2 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 PDK2 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 PDK2 immunoprecipitation

  • Tagged overexpression: HEK293T FLAG/HA-PDK2 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 PDK2 can differ in dosage, splicing, and compartmentation—in organoids/PDX, record passage, matrix, and drug history.

Quick search presets

PDK2-related antibodies (keyword-biased)

Adds PDK2 keyword bias atop the 细胞代谢 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 cellular metabolism hub for neighboring targets—cross-check PI3K, MAPK, and transmembrane transport pages as needed.