InedPage 16 of(page number not for citation purposes)BMC Genomics 2009…
페이지 정보
작성자 Lori 작성일23-09-29 14:03 조회38회 댓글0건관련링크
본문
InedPage 16 of(page number not for citation purposes)BMC Genomics 2009, 10:http://www.biomedcentral.com/1471-2164/10/Sequence Data All EST sequences described in this article have been deposited in the dbEST division of GenBank under the accession numbers [GenBank:GO 479265] - [GenBank: GO484340]. The mRNA and gDNA sequences of GHF5 and PL3 have been deposited in the DDBJ under the accession numbers [DDBJ: AB495300 (Aa-eng-1 mRNA)], [DDBJ:AB495301 (Aa-eng-1 gDNA)], [DDBJ:AB495302 (Aa-eng-2 mRNA)], [DDBJ:AB495303 (Aa-eng-2 gDNA)], [DDBJ:AB495304 (Aa-pel-1 mRNA)], [DDBJ:AB495305 (Aa-pel-1 gDNA)], [DDBJ:AB495306 (Aa-Pel-2 mRNA)] and [DDBJ:AB495307 (Aa-pel-2 gDNA).AcknowledgementsThe authors thank Asuka Shichiri for technical assistance. NK is supported by Japan Society for the Promotion of D(+)-Galactosamine (hydrochloride) Science (JSPS) Postdoctoral Fellowship for foreign researchers. TK has been funded by Japanese Ministry of Education, Science, Sports and Culture, Grant-in-Aid for Encouragement of Young Scientists (B) 18780032. JTJ is supported by Scottish Executive Environment and Rural Affairs Department. This work was supported by a grant to TK and JTJ from the Royal Society of Edinburgh and by funding through ERASMUS MUNDUS programme 2008-102 (EUMAINE).
Jochim et al. Proteome Science 2011, 9:48 http://www.proteomesci.com/content/9/1/RESEARCHOpen AccessImpact of clostridial glucosylating toxins on the proteome of colonic cells determined by isotopecoded protein labeling and LC-MALDINelli Jochim, Ralf Gerhard, Ingo Just and Andreas Pich*AbstractBackground: The anaerobe Clostridium difficile produces two major virulence factors toxin A and B that inactivate Rho proteins by glucosylation of a pivotal threonine residue. Purified toxins induce reorganization of the cytoskeleton and cell death in colonic cells. Whether all toxin effects on target cells depend on catalytic glucosyltransferase activity is unclear at present. Thus, we conducted a proteome approach to compare the protein profile of target cells treated either with wild type toxin A (rTcdA wt) or with a catalytically inactive mutant toxin A (mutant rTcdA). Relative protein quantification was feasible using isotope-coded protein labeling techniques (ICPL) and mass spectrometry (LC-MALDI). Results: Altogether we found a significant differential expression of thirty proteins after treatment with rTcdA wt or mutant rTcdA. Mutant rTcdA caused up-regulation of seven proteins and sixteen proteins were responsive to rTcdA wt after 5 h. Long-term effect of rTcdA wt on protein expression was the down-regulation of eleven proteins. Upor down-regulation of several proteins PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/16989806 was verified by western blot analysis confirming the MS results. Conclusion: Our results indicate incubation time-dependent effects of the clostridial glucosylating toxin A on colonic cells. The rTcdA wt impact more cellular functions than actin cytoskeleton reorganization and apoptosis. Furthermore, these data give insight into glucosyltransferase independent effects of clostridial glucosylating toxins on target cells after short incubation time. Additionally, our data reveal pro-inflammatory and proliferative effects of mutant rTcdA after short-term incubation. Keywords: C. difficile-associated diarrhea, colonic cells, ICPLTM, relative quantification, Toxin ABackground Clostridium difficile is a spore-forming anaerobe, which produces two major virulence factors, Toxin A (TcdA) and Toxin B (TcdB) [1]. TcdA and TcdB are the causative agents of the C. diff.
Jochim et al. Proteome Science 2011, 9:48 http://www.proteomesci.com/content/9/1/RESEARCHOpen AccessImpact of clostridial glucosylating toxins on the proteome of colonic cells determined by isotopecoded protein labeling and LC-MALDINelli Jochim, Ralf Gerhard, Ingo Just and Andreas Pich*AbstractBackground: The anaerobe Clostridium difficile produces two major virulence factors toxin A and B that inactivate Rho proteins by glucosylation of a pivotal threonine residue. Purified toxins induce reorganization of the cytoskeleton and cell death in colonic cells. Whether all toxin effects on target cells depend on catalytic glucosyltransferase activity is unclear at present. Thus, we conducted a proteome approach to compare the protein profile of target cells treated either with wild type toxin A (rTcdA wt) or with a catalytically inactive mutant toxin A (mutant rTcdA). Relative protein quantification was feasible using isotope-coded protein labeling techniques (ICPL) and mass spectrometry (LC-MALDI). Results: Altogether we found a significant differential expression of thirty proteins after treatment with rTcdA wt or mutant rTcdA. Mutant rTcdA caused up-regulation of seven proteins and sixteen proteins were responsive to rTcdA wt after 5 h. Long-term effect of rTcdA wt on protein expression was the down-regulation of eleven proteins. Upor down-regulation of several proteins PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/16989806 was verified by western blot analysis confirming the MS results. Conclusion: Our results indicate incubation time-dependent effects of the clostridial glucosylating toxin A on colonic cells. The rTcdA wt impact more cellular functions than actin cytoskeleton reorganization and apoptosis. Furthermore, these data give insight into glucosyltransferase independent effects of clostridial glucosylating toxins on target cells after short incubation time. Additionally, our data reveal pro-inflammatory and proliferative effects of mutant rTcdA after short-term incubation. Keywords: C. difficile-associated diarrhea, colonic cells, ICPLTM, relative quantification, Toxin ABackground Clostridium difficile is a spore-forming anaerobe, which produces two major virulence factors, Toxin A (TcdA) and Toxin B (TcdB) [1]. TcdA and TcdB are the causative agents of the C. diff.
댓글목록
등록된 댓글이 없습니다.