USP36 Antibody, FITC conjugated

Mechanistic Insights from Research

USP36 antibodies, including fluorescent conjugates, have been critical in elucidating its roles in:

Apoptosis Regulation

• USP36 stabilizes survivin and cIAP1 by removing K48- and K11-linked ubiquitin chains, respectively, inhibiting proteasomal degradation. Co-immunoprecipitation (Co-IP) using anti-USP36 antibodies confirmed its direct interaction with survivin and cIAP1 in colorectal cancer models .

• Functional studies show USP36 knockdown increases apoptosis, while overexpression reduces caspase-3 activation .

Cancer Progression

• In esophageal squamous cell carcinoma (ESCC), USP36 stabilizes YAP by deubiquitinating K48-linked chains, promoting tumor growth and metastasis. Anti-USP36 antibodies validated its nuclear localization and interaction with YAP .

• High USP36 expression correlates with poor differentiation and YAP upregulation in clinical ESCC samples .

Applications in Experimental Workflows

• Immunofluorescence (IF): FITC conjugation enables subcellular localization studies (e.g., nuclear/cytoplasmic USP36 distribution in ESCC ).

• Flow Cytometry: Quantify USP36 expression in live cells (intracellular staining protocols required).

• Co-IP & Ubiquitination Assays: Isolate USP36 complexes to study its deubiquitinase activity .

Validation and Quality Control

• Specificity: Verified via siRNA-mediated USP36 knockdown, showing reduced signal in WB/IF .

• Cross-Reactivity: Limited to cited species; non-reactive with avian or invertebrate homologs .

• Batch Consistency: Protein G-purified antibodies ensure minimal lot-to-lot variability .

Research Implications

Targeting USP36 with inhibitory antibodies or small molecules could disrupt oncogenic pathways (e.g., Hippo/YAP in ESCC or survivin/cIAP1 in colorectal cancer ). FITC-conjugated antibodies enable real-time tracking of USP36 dynamics during therapeutic interventions.