Sökning: id:"swepub:oai:DiVA.org:liu-99623" > Proteasomal degrada...
Fältnamn | Indikatorer | Metadata |
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000 | 02572naa a2200301 4500 | |
001 | oai:DiVA.org:liu-99623 | |
003 | SwePub | |
008 | 131018s2002 | |||||||||||000 ||eng| | |
024 | 7 | a https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-996232 URI |
024 | 7 | a https://doi.org/10.1128/IAI.70.8.4053-4058.20022 DOI |
040 | a (SwePub)liu | |
041 | a engb eng | |
042 | 9 SwePub | |
072 | 7 | a ref2 swepub-contenttype |
072 | 7 | a art2 swepub-publicationtype |
100 | 1 | a Lerm, Mariau Albert-Ludwigs-Universität Freiburg, Germany4 aut0 (Swepub:liu)marle69 |
245 | 1 0 | a Proteasomal degradation of cytotoxic necrotizing factor 1-activated rac |
264 | 1 | b American Society for Microbiology,c 2002 |
338 | a print2 rdacarrier | |
520 | a The cytotoxic necrotizing factor 1 (CNF1) from Escherichia coli has been shown to activate members of the Rho family by deamidation of glutamine 63. This amino acid is essential for hydrolysis of GTP, and any substitution results in a constitutively active Rho. Activation of Rho induces the formation of stress fibers, filopodia, and membrane ruffles due to activation of RhoA, Cdc42, and Rac, respectively. Here we show that the level of endogenous Rac decreased in CNF1-treated HEK293 and HeLa cells. The amount of mRNA remained unaffected, leaving the possibility that Rac is subject to proteolytic degradation. Treatment of cells with lactacystin, an inhibitor of the 26S proteasome, protected Rac from degradation. We have previously shown that CNF1 activates the c-Jun N-terminal kinase (JNK) only transiently in HeLa cells (M. Lerm, J. Selzer, A. Hoffmeyer, U. R. Rapp, K. Aktories, and G. Schmidt, Infect. Immun. 67:496-503, 1998). Here we show that CNF1-induced JNK activation is stabilized in the presence of lactacystin. The data indicate that Rac is degraded by a proteasome-dependent pathway in CNF1-treated cells. | |
700 | 1 | a Pop, Mariusu Albert-Ludwigs-Universität Freiburg, Germany4 aut |
700 | 1 | a Fritz, Gerhardu Institut für Toxikologie, Mainz, Germany4 aut |
700 | 1 | a Aktories, Klausu Albert-Ludwigs-Universität Freiburg, Germany4 aut |
700 | 1 | a Schmidt, Gudulau Albert-Ludwigs-Universität Freiburg, Germany4 aut |
710 | 2 | a Albert-Ludwigs-Universität Freiburg, Germanyb Institut für Toxikologie, Mainz, Germany4 org |
773 | 0 | t Infection and Immunityd : American Society for Microbiologyg 70:8, s. 4053-4058q 70:8<4053-4058x 0019-9567x 1098-5522 |
856 | 4 8 | u https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-99623 |
856 | 4 8 | u https://doi.org/10.1128/IAI.70.8.4053-4058.2002 |
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