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Segmental helical motions and dynamical asymmetry modulate histidine kinase autophosphorylation.
Mechaly AE, Sassoon N, Betton JM, Alzari PM. Mechaly AE, et al. Among authors: sassoon n. PLoS Biol. 2014 Jan 28;12(1):e1001776. doi: 10.1371/journal.pbio.1001776. eCollection 2014 Jan. PLoS Biol. 2014. PMID: 24492262 Free PMC article.
Structural Coupling between Autokinase and Phosphotransferase Reactions in a Bacterial Histidine Kinase.
Mechaly AE, Soto Diaz S, Sassoon N, Buschiazzo A, Betton JM, Alzari PM. Mechaly AE, et al. Among authors: sassoon n. Structure. 2017 Jun 6;25(6):939-944.e3. doi: 10.1016/j.str.2017.04.011. Epub 2017 May 25. Structure. 2017. PMID: 28552574 Free article.
Crystal structure of a defective folding protein.
Saul FA, Mourez M, Vulliez-Le Normand B, Sassoon N, Bentley GA, Betton JM. Saul FA, et al. Among authors: sassoon n. Protein Sci. 2003 Mar;12(3):577-85. doi: 10.1110/ps.0235103. Protein Sci. 2003. PMID: 12592028 Free PMC article.
Formation of active inclusion bodies in the periplasm of Escherichia coli.
Arié JP, Miot M, Sassoon N, Betton JM. Arié JP, et al. Among authors: sassoon n. Mol Microbiol. 2006 Oct;62(2):427-37. doi: 10.1111/j.1365-2958.2006.05394.x. Mol Microbiol. 2006. PMID: 17020581 Free article.
Conformational plasticity of the response regulator CpxR, a key player in Gammaproteobacteria virulence and drug-resistance.
Mechaly AE, Haouz A, Sassoon N, Buschiazzo A, Betton JM, Alzari PM. Mechaly AE, et al. Among authors: sassoon n. J Struct Biol. 2018 Nov;204(2):165-171. doi: 10.1016/j.jsb.2018.08.001. Epub 2018 Aug 4. J Struct Biol. 2018. PMID: 30086390
Tertiary structure-dependence of misfolding substitutions in loops of the maltose-binding protein.
Raffy S, Sassoon N, Hofnung M, Betton JM. Raffy S, et al. Protein Sci. 1998 Oct;7(10):2136-42. doi: 10.1002/pro.5560071010. Protein Sci. 1998. PMID: 9792100 Free PMC article.
Moving the loop mutation from the N- to the C-domain eliminated the in vivo misfolding step that led to the formation of inclusion bodies. ...These results strongly support the notion that the formation of super-secondary structures of the N-domain is a rate-limitin …
Moving the loop mutation from the N- to the C-domain eliminated the in vivo misfolding step that led to the formation of inclusion bo …
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