Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0043167 (pertussis)
 19,595 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The MCD peptide in bee venom induces degranulation in mast cells. The internal calcium concentration of mast cells increased and remained high following MCD stimulation. This calcium increase was blocked by pertussis toxin (Ptx) treatment, suggesting that MCD peptide activates Ptx-sensitive G-protein. Even in the absence of external calcium in the incubation medium, the calcium concentration increased by MCD treatment, but soon returned to the original level. D-MCD, the optical isomer of the MCD peptide, also increased the internal calcium concentration through a Ptx-sensitive pathway. We suggest that cationic clusters at one side of the surface are more important in activating the G-protein than the alpha-helix conformation.
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PMID:Mast cell degranulating (MCD) peptide and its optical isomer activate GTP binding protein in rat mast cells. 190 86

Bacteria of the Bordetella genus cause respiratory tract infections. Both broad host range (e.g. Bordetella bronchiseptica) and human-adapted (e.g. Bordetella pertussis) strains produce a surface-exposed and secreted protein called filamentous haemagglutinin (FHA) that functions in adherence and immunomodulation. Previous studies using B. pertussis and cultured mammalian cells identified several FHA domains with potential roles in host cell interactions, including an Arg-Gly-Asp (RGD) triplet that was reported to bind integrins on epithelial cells and monocytes to activate host signalling pathways. We show here that, in contrast to our previous report, the fhaB genes of B. pertussis and B. bronchiseptica are functionally interchangeable, at least with regard to the various in vitro and in vivo assays investigated. This result is significant because it indicates that information obtained studying FHA using B. bronchiseptica and natural-host animal models should apply to B. pertussis FHA as well. We also show that the C-terminus of mature FHA, which we name the MCD, mediates adherence to epithelial and macrophage-like cells and is required for colonization of the rat respiratory tract and modulation of the inflammatory response in mouse lungs. We could not, however, detect a role for the RGD in any of these processes.
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PMID:Natural-host animal models indicate functional interchangeability between the filamentous haemagglutinins of Bordetella pertussis and Bordetella bronchiseptica and reveal a role for the mature C-terminal domain, but not the RGD motif, during infection. 1922 Jul 44

The chemokine receptor CCR5 has been shown to be targeted to cholesterol- and sphingolipid-rich membrane microdomains. Here we elucidate the effects of membrane fluidity on CCR5 signalling and expression using the monocytic THP-1 cells. MCD treatment of THP-1 cells, which removes nearly all cholesterol from the plasma membrane, leads to an increase in the signalling properties of CCR5. In contrast, the prevention of cholesterol production with lovastatin and simvastatin decreases the release of intracellular calcium and also decreases receptor cell surface expression. The loss of response in lovastatin treated cells can be rescued by MCD addition, which shows that the cholesterol content in the membrane is only one factor in determining the amount of receptor response. We show that CCR5 signalling is dependent on thapsigargin-sensitive Ca2+ stores and on activation of ryanodine receptors as well as InsP3 receptors or store-operated channels. Cholesterol depletion with MCD changes the thapsigargin sensitivity in THP-1 cells and also alters receptor-G-protein coupling towards pertussis toxin (PTX) independent G-proteins. Cholesterol removal by MCD in THP-1 cells has far reaching consequences for receptor activation and signalling and emphasises the need for a clearer understanding of how membrane fluidity affects receptor signalling events.
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PMID:Distinct modes of molecular regulation of CCL3 induced calcium flux in monocytic cells. 1952 56