Disease relevance of Fstl3

• We found that homozygous FSTL3 knockout adults developed a distinct group of metabolic phenotypes, including increased pancreatic islet number and size, beta cell hyperplasia, decreased visceral fat mass, improved glucose tolerance, and enhanced insulin sensitivity, changes that might benefit obese, insulin-resistant patients [1].

High impact information on Fstl3

• FSTL3 deletion reveals roles for TGF-beta family ligands in glucose and fat homeostasis in adults [1].
• Immunohistochemical observations showed that positive signals of FLRG protein were colocalized in glial fibrillary acidic protein-positive reactive astroglial cells located in damaged regions after a penetrating injury [2].
• To understand the expression level of FLRG in brain tissue, we examined whether primary neurons and glial cells from rat embryos express FLRG mRNA and produce its protein product [2].
• A novel activin binding protein, follistatin-related gene (FLRG) was identified [3].
• Immunohistochemical analysis shows that FLRG is distributed in spermatogenic cells of the testis, renal tubules, epithelial cells of the lung, and myocardium [3].

Biological context of Fstl3

• This combination of phenotypes appears to arise from increased activin and myostatin bioactivity in specific tissues resulting from the absence of the FSTL3 antagonist [1].

Other interactions of Fstl3

• As an extracellular regulatory protein, we have identified a novel follistatin-like protein, named follistatin-related gene (FLRG) [4].

Analytical, diagnostic and therapeutic context of Fstl3

• Moreover, changes in expression levels of FLRG mRNA and protein in brain tissue were also analyzed after a penetrating injury, using quantitative polymerase chain reactin (PCR) and immunohistochemical methods [2].

References