FGF signaling inhibits chrondrocyte proliferation and regulates bone development through the STAT-1 pathway

Article Abstract:

FGF signaling, FGFs being a large family of fibroblast growth factors, regulates bone development through the STAT-1 pathway and inhibits chrondrocyte proliferation. Several genetic forms of human dwarfism have been linked to activating mutations in FGF receptor 3, indicating that FGF signaling has a vital role in chondrocyte maturation and development of the skeleton. The mechanisms by which FGFs affect chondrocyte proliferation and differentiation are not well understood. Activation of FGF signaling cuts down chondrocyte proliferation in a rat chondrosarcoma cell line and in primary murine chondrocytes. Primary chondrocytes from STAT-1 knock-out mice have been used to give genetic evidence that STAT-1 function is needed for the FGF mediated growth inhibition. It seems STAT-1 mediated downregulation of chondrocyte proliferation by FGF signaling is a homeostatic mechanism that ensures harmonious bone morphogenesis and development.

Bones, Growth factors, Dwarfism, Cartilage cells, Chondrosarcoma

---

ebi regulates epidermal growth factor receptor signaling pathways in Drosophila

Article Abstract:

Mutations in a gene called ebi were identified in screening for mutations that affect eye development. Genetic analysis found that ebi functions in EGFR pathways regulating aspects of gametogenesis and in imaginal disc development. The newly identified gene is quite homologous to proteins in plants, yeast and humans and is related structurally to Cdc4/Sel-10/Slimb. It has been shown that ebi is necessary in R7 development for down-regulating Ttk88 responding to epidermal growth factor (EGFR) signals. Mutations in ebi (ital) and Egfr (ital) give rise to similar phenotypes. They interact genetically, and ebi regulates EGFR receptor signaling pathways in Drosophila. The new gene does not have genetic interactions with other RTKs or with components of the canonical Ras/MAP kinase pathway.

Proteins, Epidermal growth factor, Epidermal growth factors, Protein denaturation

---

The subcellular localization of PBX1 and EXD proteins depends on nuclear import and export signals and is modulated by association with PREP1 and HTH

Article Abstract:

Localization of PBX1 and EXD proteins in a cell depends on nuclear import/export signals and is changed by being associated with HTH and PREP1. Nuclear localization of the proteins Extradenticle (EXD) and PBX1 is restricted regionally during mammalian and Drosophila development. Localization in the cell of EXD, PBS and their partners PREP1 and Homothorax (HTH) have been studied in varying cell contexts. PBX1 and EXD are in the nucleus in mouse fibroblasts but not in Drosophila Schneider cells. It is proposed that heterodimerization with HTH/PREP brings on nuclear translocation of EXD and PBX1 in certain cell contexts by preventing their nuclear export.

Italy, Drosophila, Cell nuclei, Cell nucleus

Similar abstracts:

• Abstracts: Yan functions as a general inhibitor of differentiation and is negatively regulated by activation of the Ras1/MAPK pathway
• Abstracts: Translational regulation in development. Rethinking the microprocessor. Targeted mRNA degradation by double-stranded RNA in vitro
• Abstracts: Cytosine methylation and the unequal developmental potentials of the oocyte and sperm genomes. The molecular basis of vascular disorders
• Abstracts: A forkhead gene, FoxE3, is essential for lens epithelial proliferation and closure of the lens vesicle
• Abstracts: Fat distribution during childhood and adolescence: implications for later health outcomes. Variation in subcutaneous adipose tissue distribution associated with age, sex, and maturation

This website is not affiliated with document authors or copyright owners. This page is provided for informational purposes only. Unintentional errors are possible.