Rabbit Anti-Human DKK4 Polyclonal Antibody

OBJECTIVE: Ovarian cancer is one of the most common causes of cancer-related deaths in women. Many studies show that dys-regulated gene expression plays a key role in tumorigenesis and development. Therefore, a comprehensive understanding of ovarian serous cystadenocarcinoma survival prognosis is needed. PATIENTS AND METHODS: A large number of high-dimensional RNA-sequencing files and clinical datasets collected from the Genomic Data Commons Data Portal were utilized to identify novel potential biomarkers for determining the prognosis of patients with ovarian serous cystadenocarcinoma (OVSC). We adopted a new strategy to identify these biomarkers by integrating co-expression network analysis and the Kaplan-Meier estimation with a non-parametric bootstrapping procedure. RESULTS: Functional enrichment analysis of gene modules of interest revealed several dys-regulated genes in OVSC. suggesting a close relationship between hormones and angiogenesis. In combination with this comprehensive approach, 14 genes, including ABCA10, DCX, LRRC30, ALX4, DKK4, SGCZ, ANKS4B, FHL5, SPRR2F. CHRNG. GABRR1. STMN2, CRHBP. and GSTM5. were shown to serve as candidate biomarkers for predicting the prognosis of patients with OVSC. CONCLUSIONS: The current study identified several valuable prognostic biomarkers and several potential therapeutic targets for treating OVSC.

The mouse hair coat comprises protective "primary'' and thermo-regulatory "secondary'' hairs. Primary hair formation is ectodysplasin (Eda) dependent, but it has been puzzling that Tabby (Eda(-/y)) mice still make secondary hair. We report that Dickkopf 4 (Dkk4), a Wnt antagonist, affects an auxiliary pathway for Eda-independent development of secondary hair. A Dkk4 transgene in wild-type mice had no effect on primary hair, but secondary hairs were severely malformed. Dkk4 action on secondary hair was further demonstrated when the transgene was introduced into Tabby mice: the usual secondary follicle induction was completely blocked. The Dkk4-regulated secondary hair pathway, like the Eda-dependent primary hair pathway, is further mediated by selective activation of Shh. The results thus reveal two complex molecular pathways that distinctly regulate subtype-based morphogenesis of hair follicles, and provide a resolution for the longstanding puzzle of hair formation in Tabby mice lacking Eda.