KCS17 Antibody

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Product Specs

Buffer
Preservative: 0.03% ProClin 300; Constituents: 50% Glycerol, 0.01M PBS, pH 7.4
Form
Liquid
Lead Time
14-16 weeks (made-to-order)
Synonyms
KCS17; KCS2; At4g34510; T4L20.90; 3-ketoacyl-CoA synthase 17; KCS-17; Very long-chain fatty acid condensing enzyme 17; VLCFA condensing enzyme 17
Target Names
KCS17
Uniprot No.

Target Background

Function
This antibody targets an enzyme active on saturated acyl-CoAs with chain lengths up to C22. It mediates the synthesis of very-long-chain fatty acids (VLCFAs) ranging from 20 to 26 carbons (e.g., C20:1, C20, C24, C26).
Database Links

KEGG: ath:AT4G34510

STRING: 3702.AT4G34510.1

UniGene: At.27519

Protein Families
Chalcone/stilbene synthases family
Subcellular Location
Membrane; Multi-pass membrane protein.
Tissue Specificity
Expressed in flowers.

Q&A

FAQs for Researchers on K17 Antibody in Academic Research

Advanced Research Questions

What molecular mechanisms link K17 to T cell trafficking in inflammatory skin diseases?

  • K17 promotes CCL20 production in keratinocytes via STAT3 activation. Nuclear translocation of K17 (dependent on NLS/NES sequences) facilitates STAT3 binding, amplifying CCL20 secretion and recruiting CCR6+ T cells .

  • Key experimental steps:

    • Silence K17 via siRNA in keratinocytes and measure CCL20 levels via ELISA.

    • Co-immunoprecipitation to confirm K17-STAT3 interaction .

How can discrepancies in K17’s utility as a biomarker be resolved?

  • Variable antibody detection: In Kawasaki disease (KD), anti-HSP7C (a related heat shock protein) antibodies were detected in only 60% of patients via ELISA, suggesting subtype heterogeneity . For K17, IHC scoring systems (e.g., H-score) and standardized thresholds (e.g., ≥30% tumor positivity) improve reproducibility .

  • Cohort stratification: Analyze K17 expression alongside PD-L1 status, tumor mutational burden, and clinical variables (e.g., prior therapies) .

Does K17 influence resistance to cancer immunotherapy?

  • Clinical evidence: In head and neck squamous cell carcinoma (HNSCC), high K17 expression correlates with shorter progression-free survival (PFS) post-immune checkpoint blockade (ICB).

    BiomarkerResponse Rate (Low K17)Response Rate (High K17)Median PFS
    K17 IHC42%12%6.2 vs. 2.1 months
  • Mechanistic insight: K17 may drive an immunosuppressive tumor microenvironment by recruiting regulatory T cells or upregulating PD-L1 .

Methodological Challenges & Solutions

How to address variability in K17 antibody performance across assays?

  • Validation protocols:

    • Use CRISPR-edited K17-KO cell lines as negative controls .

    • Compare multiple antibody clones (e.g., EP1607I vs. EPR16894) in parallel assays .

  • Multiplex platforms: Combine IHC with spatial transcriptomics to map K17 expression within tumor-immune niches .

What in vivo models best recapitulate K17’s role in autoimmune pathologies?

  • K17-transgenic mice: Overexpress human K17 in keratinocytes to study psoriasis-like inflammation.

  • Adoptive T cell transfer: Isolate CCR6+ T cells from K17-driven CHS models and track migration to CCL20-rich sites .

Data Contradiction Analysis

  • Example: While K17 promotes inflammation in allergic contact dermatitis , it is paradoxically linked to immune evasion in HNSCC .

    • Resolution: Tissue-specific context matters. In stroma-rich tumors, K17 may recruit immunosuppressive cells, whereas in skin, it amplifies effector T cell responses.

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