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Enamelin (Enam) is essential for amelogenesis: ENU-induced mouse mutants as models for different clinical subtypes of human amelogenesis imperfecta (AI).
It is reported here that the Enam gene is essential for amelogenesis, and that mice with different point mutations at Enam may provide good animal models to study the different clinical subtypes of AI.
Implementation of the modified-SHIRPA protocol for screening of dominant phenotypes in a large-scale ENU mutagenesis program
Using modified-SHIRPA, dominant phenotypes of more than 10,000 G1 progeny generated by crossing DBA/2J females with ENU-treated C57BL/6J males are screened and some independent mutant lines exhibited similar phenotypes, suggesting that they may represent alleles of the same gene or mutations in the same genetic pathway.
A novel dominant-negative mutation in Gdf5 generated by ENU mutagenesis impairs joint formation and causes osteoarthritis in mice.
A critical role of GDF5 in joint formation and the development of OA is highlighted, and this mouse should serve as a good model for OA.
Fibrocystin interacts with CAML, a protein involved in Ca2+ signaling.
Inhibition of prostasin secretion by serine protease inhibitors in the kidney.
It is suggested that a serine protease-sensitive mechanism is involved in the secretion of prostasin in vitro as well as in vivo, and could account for the side effects of hyponatremia and/or hyperkalemia that are found sometimes in patients treated with NM.
Immunomodulatory constituents from three ascomycetes, Gelasinospora heterospora, G. multiforis, and G. longispora.
Three new 2-pyrones (2H-pyran-2-ones) called multiforisins G (3), H (1), and I (4), and a known hexaketide sordarial (2) have been isolated from an Ascomycete Gelasinospora heterospora. Among them,
Inhibition of prostasin expression by TGF-beta1 in renal epithelial cells.
The findings indicate the possibility that TGF-beta1 transcriptionally inhibits prostasin expression by the induction of IkappaBalpha and the subsequent inhibition of NF-kappaB/Rel activity in M-1 cells, and suggest the possibility of TGF -beta1 might inhibit sodium reabsorption through a reduction in prostasinexpression andsequent inhibition of ENaC activity.
Role of ceramide in Ca2+-sensing receptor-induced apoptosis Published, JLR Papers in Press, April 1, 2005. DOI 10.1194/jlr.M500071-JLR200
The involvement of the CaR is reported in stimulating programmed cell death via a pathway involving GTP binding protein alpha subunit (Gαi)-dependent ceramide accumulation, activation of stress-activated protein kinase/c-Jun N-terminal kinase, c-Jun phosphorylation, caspase-3 activation, and DNA cleavage.