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S Yakar

Publications and source records attributed to S Yakar.

20 records · Page 2Linked to original sources

Growth hormone (GH) stimulates insulin-like growth factor-I (IGF-I) and IGF-binding protein (IGFBP)-2 gene expression in spleens of juvenile rats.

Growth and development of the spleen involves the growth hormone (GH)/insulin-like growth factor-I (IGF-I) axis. To evaluate the molecular mechanism of these effects we studied the effect of hypophysectomy (Hx) and GH replacement therapy on the expression of IGF-I, the IGF-I receptor and IGF-binding protein-2 (IGFBP-2) in juvenile rats. Hx resulted in a 30% reduction in body weight. GH replacement therapy for seven days partially prevented these effects. IGF-I mRNA levels were reduced 30% by Hx, IGFBP-2 mRNA levels fell 50% whereas IGF-I receptor mRNA levels were unaffected. GH therapy prevented the reduction in IGF-I and IGFBP-2 mRNA levels. These results suggest that the GH effect on splenic growth and development is via local (paracrine) IGF-I expression, in addition to any effect by circulating (endocrine) IGF-I.

Animals↗

Direct evidence for SAA deposition in tissues during murine amyloidogenesis.

To study the mechanism of amyloid deposition, the nature of amyloid proteins formed in experimental murine amyloidosis, was examined. Spleen specimens, 15-60 mg, were homogenized and extracted using aqueous acidic acetonitrile, in a recently developed procedure, making it possible to obtain amyloid proteins from minute amounts of tissue. The extracted material, 1.5-4 mg, was analysed by Western blotting and ELISA using antibodies recognizing differentially proteins AA and SAA. Two immunoreactive proteins of 8 and 12 KDa were isolated and subjected to amino acid analysis and N-terminal sequence determination. The results of immunochemical and chemical examination showed that the 8 and 12 KDa proteins represented proteins AA and SAA, respectively. The data obtained provide new direct evidence for SAA in tissues during murine amyloidogenesis.

Amino Acid Sequence↗