Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cytokine-induced apoptosis inhibitor (CIAP) is a novel antiapoptotic molecule, which is different to inhibitor of apoptosis protein or B-cell lymphoma 2. CIAP was originally identified as a molecule that conferred resistance to apoptosis induced by growth factor starvation. However, it remains to be undercharacterized in schistosomes. Here, we molecularly characterize a novel cytokine-induced apoptosis inhibitor from Schistosoma japonicum (SjCIAP). The transcription of the SjCIAP occurred at all of developmental stages investigated including eggs, cercariae, schistosomula, and adult schistosomes. Functional assay indicated that the SjCIAP could inhibit caspase activity in either human cell lines or schistosome lysates. Our preliminary results suggest that the SjCIAP may play important roles in parasitic living and development by regulating apoptosis, and drug target of SjCIAP might be a potential for schistosomiasis control.
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PMID:Molecular characterization of a cytokine-induced apoptosis inhibitor from Schistosoma japonicum. 2293 40

Schistosoma japonicum insulin receptors (SjIRs) have been identified as encouraging vaccine candidates. Interrupting or blocking the binding between host insulin and the schistosome insulin receptors (IRs) may result in reduced glucose uptake leading to starvation and stunting of worms with a reduction in egg output. To further understand how schistosomes are able to exploit host insulin for development and growth, and whether these parasites and their mammalian hosts compete for the same insulin source, we identified insulin binding sites on the SjIRs. Based on sequence analysis and the predicted antigenic structure of the primary sequences of the SjIRs, we designed nine and eleven peptide analogues from SjIR-1 and SjIR-2, respectively. Using the Octet RED system, we identified analogues derived from SjIR-1 (10) and SjIR-2 (20, 21 and 22) with insulin-binding sequences specific for S. japonicum. Nevertheless, the human insulin receptor (HIR) may compete with the SjIRs in binding human insulin in other positions which are important for HIR binding to insulin. However, no binding occurred between insulin and parasite analogues derived from SjIR-1 (2, 7 and 8) and SjIR-2 (14, 16 and 18) at the same locations as HIR sequences which have been shown to have strong insulin binding affinities. Importantly, we found two analogues (1 and 3), derived from SjIR-1, and two analogues (13 and 15) derived from SjIR-2, were responsible for the major insulin binding affinity in S. japonicum. These peptide analogues were shown to have more than 10 times (in KD value) stronger binding capacity for human insulin compared with peptides derived from the HIR in the same sequence positions. Paradoxically, analogues 1, 3, 13 and 15 do not appear to contain major antigenic determinants which resulted in poor antibody responses to native S. japonicum protein. This argues against their future development as peptide-vaccine candidates.
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PMID:Identification of Host Insulin Binding Sites on Schistosoma japonicum Insulin Receptors. 2744 98