FUT11 Antibody

Here’s a structured collection of research-focused FAQs for FUT11 antibodies, synthesized from peer-reviewed studies and technical specifications across multiple sources:

Advanced Research Challenges

How to resolve conflicting Western blot results for FUT11?

Conflicting bands (e.g., 55 vs. 56 kDa) may arise from:

• Isoforms: FUT11 has two isoforms (56 kDa canonical vs. truncated variants) ( ).

• Glycosylation: FUT11 is heavily glycosylated; treat lysates with PNGase F to confirm core protein size ( ).

• Cross-reactivity: Validate using FUT3/FUT5/FUT8 knockout models due to 1% homology overlap ( ).

What methodologies identify FUT11’s functional role in hypoxia-driven cancer progression?

• Hypoxia Mimicry: Treat pancreatic cancer cells (e.g., AsPC-1) with CoCl₂ (200 μM, 24 hr) to induce HIF1α-mediated FUT11 upregulation ( ).

• Functional Assays:

  • Proliferation: CCK-8/EDU assays show FUT11 knockdown reduces growth under hypoxia (HR = 1.884, p < 0.05) ( ).

  • Migration: Transwell assays reveal 40–60% reduction in migratory capacity post-FUT11 silencing ( ).

How to investigate FUT11’s interaction partners in signaling pathways?

• Co-Immunoprecipitation (Co-IP): Use weak RIPA buffer + protease inhibitors to preserve FUT11-PDK1 interactions ( ).

• Mass Spec Analysis: Identified 700 interactors; PDK1 (a key oncogene) co-localizes with FUT11 in pancreatic cancer models ( ).

• Ubiquitination Assays: Treat cells with cycloheximide (CHX, 50 μg/mL) to show FUT11 stabilizes PDK1 by reducing proteasomal degradation ( ).

Why does FUT11 antibody performance vary across tissue types?

Tissue-specific challenges include:

How to validate FUT11’s enzymatic activity in glycan modification studies?

• Substrate Specificity:

  • Isoform 1: Weak activity toward biantennary N-glycans ( ).

  • Isoform 2: Robust α1,3-fucosylation of Lewis X motifs ( ).

• Functional Assay: Use GDP-fucose + biantennary N-glycan acceptor (1 mM); quantify fucose transfer via HPLC ( ).