Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.1 (protein kinase)
 81,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Expression of many components of the secretory pathway in peptidergic neuroendocrine cells is precisely controlled in response to secretagogues. Regulated endocrine-specific protein (RESP18) was identified as a dopamine-regulated intermediate pituitary transcript. Although the amino acid sequence of RESP18 initially suggested that it might be a novel preprohormone, its widespread expression in peptide-producing neurons and endocrine cells and its localization to the lumen of the endoplasmic reticulum suggested that it subserves a unique function. Subtractive hybridization of a pituitary corticotrope AtT-20 cell line engineered for inducible RESP18 expression demonstrated a RESP18-dependent induction of several transcripts. Regulation of RESP18 expression in vitro and in vivo was accompanied by changes in the same transcripts. Several cDNAs encoding transcripts up-regulated by RESP18 were analyzed by DNA sequencing, searching the GenBank databases for homologous proteins, and Northern blotting. One novel clone showed a tissue distribution nearly identical to that of RESP18. One clone was identical to rat LIMK2, a protein kinase containing modular protein-protein interaction LIM (lin-11, isl-1, mec-3) domains. Another clone was similar to monomeric bacterial isocitrate dehydrogenases. Like the unfolded protein response, these data demonstrate a novel signaling pathway from the secretory pathway lumen to the nucleus. RESP18 acts as a lumicrine peptide (an intracellular luminal autocrine hormone) inducing this pathway.
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PMID:A novel neuroendocrine intracellular signaling pathway. 936 52

To achieve a better understanding of the mechanism of intimal thickening, we used a rabbit model in which aorta was denuded mechanically by a balloon catheter. Total RNA was prepared from each aorta 1, 2, 7, 14, 23, or 30 days after denudation, and from intact aorta of non-denuded control rabbits. Subsequently, using the differential display method, we identified eight genes that were expressed differently during the time course after injury. One of them, RESP18 (encoding regulated endocrine secretory protein 18), was suppressed during the acute reaction. The other seven showed increase in expression during the acute phase: the genes for hTAFII68 (human TATA-binding protein associated factor), NPAT (nuclear protein mapped to the AT locus), OSF2 (osteoblast-specific factor 2), Pyst1, casein kinase 1 alpha, integrin alpha 1, and XP-C complementing protein. Although hTAFII68, NPAT, OSF2, and Pyst1 are thought to be related to transcription, not all four are positive regulators. Considering that none of these genes had previously been reported as being implicated in intimal hyperplasia, we conclude that many known or unknown genes play roles in this process. We believe that differential display is an effective method for screening genes whose variations in expression can provide clues toward understanding the molecular mechanism of intimal hyperplasia.
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PMID:Identification by differential display of eight known genes induced during in vivo intimal hyperplasia. 960 92