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Michael G Jobling

Showing results (11-20 of 37) with videos related to

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Plos One|January 14, 2012
Type II heat-labile enterotoxins from 50 diverse Escherichia coli isolates belong almost exclusively to the LT-IIc family and may be prophage encodedMichael G Jobling, Randall K Holmes
Infection and Immunity|February 21, 2002
Mutational analysis of ganglioside GM(1)-binding ability, pentamer formation, and epitopes of cholera toxin B (CTB) subunits and CTB/heat-labile enterotoxin B subunit chimerasMichael G Jobling, Randall K Holmes
Ecosal Plus|October 8, 2015
Heat-Labile EnterotoxinsMichael G Jobling, Randall K Holmes
Traffic (Copenhagen, Denmark)|April 16, 2003
A class of mutant CHO cells resistant to cholera toxin rapidly degrades the catalytic polypeptide of cholera toxin and exhibits increased endoplasmic reticulum-associated degradationKen Teter, Michael G Jobling, Randall K Holmes
Infection and Immunity|November 24, 2004
Vesicular transport is not required for the cytoplasmic pool of cholera toxin to interact with the stimulatory alpha subunit of the heterotrimeric g proteinKen Teter, Michael G Jobling, Randall K Holmes
Genome Announcements|August 13, 2016
Complete Genome Sequence of Escherichia coli ER1821R, a Laboratory K-12 Derivative Engineered To Be Deficient in All Methylcytosine and Methyladenine Restriction SystemsMichael G Jobling, Elisabeth A Raleigh, Daniel N Frank
Infection and Immunity|March 23, 2006
The cholera toxin A1(3) subdomain is essential for interaction with ADP-ribosylation factor 6 and full toxic activity but is not required for translocation from the endoplasmic reticulum to the cytosolKen Teter, Michael G Jobling, Danielle Sentz, et al.
Infection and Immunity|October 16, 2002
Transfer of the cholera toxin A1 polypeptide from the endoplasmic reticulum to the cytosol is a rapid process facilitated by the endoplasmic reticulum-associated degradation pathwayKen Teter, Rebecca L Allyn, Michael G Jobling, et al.
Toxins|March 21, 2015
A mutational analysis of residues in cholera toxin A1 necessary for interaction with its substrate, the stimulatory G protein GsαMichael G Jobling, Lisa F Gotow, Zhijie Yang, et al.
Science (New York, N.Y.)|August 16, 2005
Structural basis for the activation of cholera toxin by human ARF6-GTPClaire J O'Neal, Michael G Jobling, Randall K Holmes, et al.
Pageof 4

Showing results (11-20 of 37) with videos related to

Sort By:
Pageof 4
Plos One|January 14, 2012
Type II heat-labile enterotoxins from 50 diverse Escherichia coli isolates belong almost exclusively to the LT-IIc family and may be prophage encodedMichael G Jobling, Randall K Holmes
Infection and Immunity|February 21, 2002
Mutational analysis of ganglioside GM(1)-binding ability, pentamer formation, and epitopes of cholera toxin B (CTB) subunits and CTB/heat-labile enterotoxin B subunit chimerasMichael G Jobling, Randall K Holmes
Ecosal Plus|October 8, 2015
Heat-Labile EnterotoxinsMichael G Jobling, Randall K Holmes
Traffic (Copenhagen, Denmark)|April 16, 2003
A class of mutant CHO cells resistant to cholera toxin rapidly degrades the catalytic polypeptide of cholera toxin and exhibits increased endoplasmic reticulum-associated degradationKen Teter, Michael G Jobling, Randall K Holmes
Infection and Immunity|November 24, 2004
Vesicular transport is not required for the cytoplasmic pool of cholera toxin to interact with the stimulatory alpha subunit of the heterotrimeric g proteinKen Teter, Michael G Jobling, Randall K Holmes
Genome Announcements|August 13, 2016
Complete Genome Sequence of Escherichia coli ER1821R, a Laboratory K-12 Derivative Engineered To Be Deficient in All Methylcytosine and Methyladenine Restriction SystemsMichael G Jobling, Elisabeth A Raleigh, Daniel N Frank
Infection and Immunity|March 23, 2006
The cholera toxin A1(3) subdomain is essential for interaction with ADP-ribosylation factor 6 and full toxic activity but is not required for translocation from the endoplasmic reticulum to the cytosolKen Teter, Michael G Jobling, Danielle Sentz, et al.
Infection and Immunity|October 16, 2002
Transfer of the cholera toxin A1 polypeptide from the endoplasmic reticulum to the cytosol is a rapid process facilitated by the endoplasmic reticulum-associated degradation pathwayKen Teter, Rebecca L Allyn, Michael G Jobling, et al.
Toxins|March 21, 2015
A mutational analysis of residues in cholera toxin A1 necessary for interaction with its substrate, the stimulatory G protein GsαMichael G Jobling, Lisa F Gotow, Zhijie Yang, et al.
Science (New York, N.Y.)|August 16, 2005
Structural basis for the activation of cholera toxin by human ARF6-GTPClaire J O'Neal, Michael G Jobling, Randall K Holmes, et al.
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