ArticleBiochemistry2012
Conformational properties of nine purified cystathionine β-synthase mutants.
Article in Biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 31 citations in OpenAlex.
- Cellular turnover and degradation of the most common missense cystathionine beta-synthase variants causing homocystinuria.Protein science : a publication of the Protein Society · 2024Article
- Molecular Mechanisms, Genotype-Phenotype Correlations and Patient-Specific Treatments in Inherited Metabolic Diseases.Journal of personalized medicine · 2023Article
- A proactive genotype-to-patient-phenotype map for cystathionine beta-synthase.Genome medicine · 2020Article
- Hydrogen sulfide: physiological properties and therapeutic potential in ischaemia.British journal of pharmacology · 2015Review
- Inter-domain communication of human cystathionine β-synthase: structural basis of S-adenosyl-L-methionine activation.The Journal of biological chemistry · 2014Article
- Structural insight into the molecular mechanism of allosteric activation of human cystathionine β-synthase by S-adenosylmethionine.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- The role of surface electrostatics on the stability, function and regulation of human cystathionine β-synthase, a complex multidomain and oligomeric protein.Biochimica et biophysica acta · 2014Article
- Reduced response of Cystathionine Beta-Synthase (CBS) to S-Adenosylmethionine (SAM): Identification and functional analysis of CBS gene mutations in Homocystinuria patients.Journal of inherited metabolic disease · 2014Article
- Mono and dual cofactor dependence of human cystathionine β-synthase enzyme variants in vivo and in vitro.G3 (Bethesda, Md.) · 2013Article
- Structural basis of regulation and oligomerization of human cystathionine β-synthase, the central enzyme of transsulfuration.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 6 institutions in 4 countries.
Funding
Abstract
Protein misfolding due to missense mutations is a common pathogenic mechanism in cystathionine β-synthase (CBS) deficiency. In our previous studies, we successfully expressed, purified, and characterized nine CBS mutant enzymes containing the following patient mutations: P49L, P78R, A114V, R125Q, E176K, R266K, P422L, I435T, and S466L. These purified mutants exhibited full heme saturation, normal tetrameric assembly, and high catalytic activity. In this work, we used several spectroscopic and proteolytic techniques to provide a more thorough insight into the conformation of these mutant enzymes. Far-UV circular dichroism, fluorescence, and second-derivative UV spectroscopy revealed that the spatial arrangement of these CBS mutants is similar to that of the wild type, although the microenvironment of the chromophores may be slightly altered. Using proteolysis with thermolysin under native conditions, we found that the majority of the studied mutants is more susceptible to cleavage, suggesting their increased local flexibility or propensity for local unfolding. Interestingly, the presence of the CBS allosteric activator, S-adenosylmethionine (AdoMet), increased the rate of cleavage of the wild type and the AdoMet-responsive mutants, while the proteolytic rate of the AdoMet-unresponsive mutants was not significantly changed. Pulse proteolysis analysis suggested that the protein structure of the R125Q and E176K mutants is significantly less stable than that of the wild type and the other mutants. Taken together, the proteolytic data shows that the conformation of the pathogenic mutants is altered despite retained catalytic activity and normal tetrameric assembly. This study demonstrates that the proteolytic techniques are useful tools for the assessment of the biochemical penalty of missense mutations in CBS.
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