Robert d pfeffer m-drol

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Annu Rev Microbiol. Subsequently, it accumulates in a discrete population of endosomes lacking classical EE markers en route to the TGN [ 65 ]. If you no longer wish to receive this email, unsubscribe using the link at the bottom of the page. External link. J Virol. Tissue receptor for cholera exotoxin: postulated structure from studies with GM1 ganglioside and related glycolipids.

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  • Retrograde transport pathways utilised by viruses and protein toxins

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    Nevertheless, the Figure points out that ligands with a common receptor eg.

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    Rapid cycling of lipid raft markers between the cell surface and Golgi complex. Nat Cell Biol. Embo J. Indeed, in a caveolin-1 cav-1 -deficient cell line human hepatoma 7 and embryonic fibroblasts from a cav-1 knockout mouse, SV40 exploits an alternative, cavindependent pathway and this alternative pathway is also available in wild-type embryonic fibroblasts [ 56 ]. There is also evidence that PEx can use the Sec61 complex for dislocation [ ].

    To date, details of ER escape mechanisms are poorly understood, beyond a likely requirement for the Sec61 translocon for toxins, but we fully expect dislocation motors for both toxins and viruses to show strong similarities.

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    Robert d pfeffer m-drol
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    Subsequently, it accumulates in a discrete population of endosomes lacking classical EE markers en route to the TGN [ 65 ]. Infect Immun.

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    . It should he noted that upoin Iv drol sis dii. iii Ii. rine c-an open on eiiher side resulting in a form of co- polymer. Methods: Survival of a national cohort of patients treated surgically for colonic and rectal cancer over a 10‐year interval was analysed. All 31 patients in.

    Apr 7, J.A; Lynne M Roberts: w@; J Michael Lord: kciwraw@ . [PMC free article] [PubMed] [CrossRef] [Google Scholar]; Lombardi D, Soldati T, Riederer MA, Goda Y, Zerial M, Pfeffer SR.
    During this early entry process, if required, activation of the toxin by furin cleavage will occur.

    Retrograde transport pathways utilised by viruses and protein toxins

    National Center for Biotechnology InformationU. In This Issue. FEBS Lett. Histochem Cell Biol. The cleaved products remain disulphide bonded in the mature toxin. ERpmodified VP1 can interact with liposomes, and by extension, probably therefore with the ER membrane, in preparation for membrane penetration.

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    At least one correctly folded protein, calreticulin, normally regarded as an ER residentcan also be unfolded to enter the cytosol from the ER, via the translocon, and refolds in the cytosol to avoid degradation [ ].

    Seen in his light, the low lysine complement of these toxins would permit avoidance of degradation, the ultimate fate of normal ERAD substrates. For influenza virus and other enveloped viruses, nucleocapsid delivery to the cytosol requires the low pH environment of the endosome to trigger exposure of a hydrophobic peptide buried within the virus fusion protein, which then stimulates fusion of the viral and endosomal membranes [ 19 ].

    Cholera toxin is exported from microsomesby the Sec61p complex. Biochem J.

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    1. This pathway appears to be very important for PEx as PEx transport is accelerated after inhibition or genetic ablation of the tyrosine kinase Src [ 79 ], which regulates KDEL-receptor distribution.

    2. ERp29 triggers a conformational change in polyomavirus to stimulate membrane binding. Major histocompatibility complex class I molecules mediate association of SV40 with caveolae.

    3. CTx B chain binds a membrane glycolipid, the ganglioside GM1 [ 2930 ] with up to 5 gangliosides being bound per holotoxin molecule, contributing to a theoretically high avidity of binding. A class of mutant CHO cells resistant to cholera toxin rapidly degrades the catalytic polypeptide of cholera toxin and exhibits increased endoplasmic reticulum-associated degradation.