Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute deficiency in pancreatic peptides (insulin, somatostatin-25, glucagon, and glucagon-like peptide) was invoked for 9-12 hr in coho, Oncorhynchus kisutch, and chinook, O. tshawytscha, salmon by administration of specific antisera raised against purified salmon hormones. Insulin-deficient fish were hyperglycemic, had diminished glycogen content in the liver (Plisetskaya et al., '88a, elevated liver triacylglycerol lipase activity, and higher concentration of plasma triiodothyronine (T3) compared to a control group of fish injected with nonspecific rabbit serum. After immunoneutralization of somatostatin-25, fish remained normoglycemic, with higher liver glycogen content, decreased lipase activity, and elevated plasma levels of insulin, while the levels of T3 declined. The induced deficiency in glucagon family peptides led to comparatively smaller changes: liver glycogen content was increased after anti-glucagon-like peptide (aGLP) injection and transient hyperglycemia was apparent following anti-glucagon (aGLU) administration. Circulating levels of insulin remained unaffected for at least 9 hr following aGLU and aGLP treatments. The velocity of pyruvate kinase at 2.5 mM phosphoenolpyruvate (V2.5) was depressed, especially after the combined administration of aGLU + aGLP. The effectiveness of immunoneutralization experiments was greatly dependent on the particular stage of the fish life cycle. Antisera against fish pancreatic peptides proved to be a suitable tool in the studies of hormonal regulation of fish metabolism.
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PMID:Metabolic changes in coho and chinook salmon resulting from acute insufficiency in pancreatic hormones. 256 43

The total sequence of a 13,021 base-pair (bp) genomic fragment containing the rat L-type pyruvate kinase (L-PK) gene was determined by "shot gun" sequencing. This fragment includes 8360 bp of the L-PK gene, plus 3193 bp of the 5'-flanking and 1468 bp of the 3'-flanking regions. Like the chicken PK-M1 gene, the rat L-PK gene exhibits a fully conserved exon-intron structure, with 11 exons and 10 introns. In the chicken M1 gene, the coding sequences are well conserved (about 70%), in particular at the level of the exons implicated in the formation of PK active sites, exons that are also partially homologous to the corresponding sequences of the yeast gene. Various types of repetitive sequences exist in the L-PK gene, especially two ID (identifier) sequences located in the second intron and the 11th exon. Elements very similar to the "cyclic AMP-dependent regulatory element" recently described in the phosphoenolpyruvate carboxykinase and somatostatin genes are found in the sequenced fragment, but far upstream (-2338) and downstream (+5788) from the cap site. Various sequences homologous to described regulatory elements (glucocorticoid regulatory elements, enhancers, potential Z-DNA) are also observed 5' and 3' of the cap site. A comparison of the 5'-flanking region of the L-PK gene with the same regions of liver-specific or non-specific, cyclic-AMP-responsive or non-responsive genes was also made. It revealed various potentially interesting features that will be used to guide a further functional study. The cap site was determined by primer extension and nuclease S1 mapping using either mature mRNA or precursor RNA as templates. With both templates the start site of transcription appeared to be microheterogeneous, 19 to 14 bp before the ATG translation initiation codon.
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PMID:Structure of the rat L-type pyruvate kinase gene. 330 48

TT-232 is a structural analogue of somatostatin exhibiting strong and selective growth-inhibitory effects, inhibition of neurogenic inflammation, as well as general anti-inflammatory and analgesic potential without the wide-ranging endocrine side effects of the parent hormone and its "traditional" analogues. The anti-inflammatory action of TT-232 is mediated through the SSTR4 receptor, and its antitumor activity is mediated through the SSTR1 receptor and by the tumor-specific isoform of pyruvate kinase. Its mechanism of action is in line with a new era of molecular medicine called signal transduction therapy, where "false" intracellular or intercellular communication is inhibited or corrected without interfering with basic cell functions and machinery. TT232 has passed phase I clinical trials without toxicity and significant side effects, and phase II studies are running for oncological and anti-inflammatory indications, respectively. This compound has the perspective to become the first drug in molecularly targeted therapy of inflammation where a combined effect of anti-inflammatory, analgesic, and neurogenic inflammation-inhibiting activity can be achieved.
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PMID:TT232, a novel signal transduction inhibitory compound in the therapy of cancer and inflammatory diseases. 1639 13