TCP10L antibodies are polyclonal or monoclonal reagents designed to detect TCP10L, a 24 kDa protein encoded by the TCP10L gene (UniProt ID: Q8TDR4). These antibodies are validated for use in western blot (WB), immunohistochemistry (IHC), immunofluorescence (IF), and ELISA. Key characteristics include:
TCP10L antibodies undergo rigorous validation to ensure specificity and reproducibility:
Western Blot: Detects TCP10L in mouse testis lysates and HCC cell lines (e.g., Hep3B, HepG2) .
Immunohistochemistry: Shows strong staining in human testis and liver tissues, with reduced expression in HCC tumors .
Functional Validation: Confirmed via knockdown/overexpression experiments in HCC models, demonstrating inverse correlation with AFP (alpha-fetoprotein) levels .
TCP10L antibodies have been pivotal in elucidating the protein’s role in HCC:
Mechanistic Studies:
TCP10L binds the AFP promoter (-981 to -821 bp) and suppresses AFP transcription via its leucine zipper (LZ) domain, as shown by chromatin immunoprecipitation (ChIP) and luciferase reporter assays .
Overexpression of TCP10L reduces AFP protein levels by 60–80% in Hep3B cells, while knockdown increases AFP expression .
Protein-Protein Interactions:
TCP10L is downregulated in 50–60% of HCC cases, correlating with larger tumor size and advanced Milan criteria .
Low TCP10L expression associates with elevated serum AFP (>20 ng/mL; P = 0.024) and poorer prognosis .
| Clinical Parameter | Correlation with TCP10L | Statistical Significance |
|---|---|---|
| Serum AFP level | Inverse (r = -0.2198) | P < 0.001 |
| Tumor size (>5 cm) | Inverse | P = 0.201 |
| Milan criteria (exceeding) | Inverse | P < 0.05 |
TCP10L recruits MAD1 to repress oncogenic pathways, inducing G1 cell cycle arrest and inhibiting tumor growth in vivo .
The LZ domain is essential for TCP10L’s function; deletion mutants (ΔLZ) fail to suppress AFP or stabilize MAD1 .