Relevant bibliographies by topics / Homocysteinylation

Academic literature on the topic 'Homocysteinylation'

Author: Grafiati
Published: 6 September 2023

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Journal articles on the topic "Homocysteinylation"

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Bełtowski, Jerzy, Grażyna Wójcicka, and Hieronim Jakubowski. "Modulation of paraoxonase 1 and protein N-homocysteinylation by leptin and the synthetic liver X receptor agonist T0901317 in the rat." Journal of Endocrinology 204, no. 2 (November 2, 2009): 191–98. http://dx.doi.org/10.1677/joe-09-0298.

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The adipose tissue hormone leptin and homocysteine (Hcy)-thiolactone are linked to the pathogenesis of atherosclerosis through their interactions with the anti-atherogenic enzyme paraoxonase 1 that has the ability to hydrolyze Hcy-thiolactone and minimizes protein N-homocysteinylation. Here we examined the relationships between hyperleptinemia, Hcy-thiolactonase, and protein N-homocysteinylation in rats. Hyperleptinemia was induced in adult rats by administration of leptin for 7 days (0.25 mg/kg twice daily s.c). We found that serum Hcy-thiolactonase was lower in hyperleptinemic than in control animals (−41.0%, P<0.001). Leptin administration increased the level of N-linked Hcy in plasma proteins (+92.9%, P<0.01), but had no effect on plasma total Hcy. These effects were not reproduced by pair-feeding. We also found that the synthetic liver X receptor (LXR) agonist, T0901317 (1 mg/kg per day) normalized Hcy-thiolactonase and protein N-homocysteinylation levels in leptin-treated rats. However, leptin-induced increase in plasma isoprostane levels (a marker of oxidative stress) was not normalized by T0901317. The NADPH oxidase inhibitor apocynin prevented leptin-induced increase in isoprostane levels but did not normalize Hcy-thiolactonase and protein N-homocysteinylation levels. These results suggest that the decreased capacity to metabolize Hcy-thiolactone and concomitant increase in protein N-homocysteinylation contribute to pro-atherogenic effect of chronic hyperleptinemia, independently of oxidative stress. LXR agonists normalize Hcy-thiolactonase levels and decrease protein N-homocysteinylation, especially under conditions associated with excess leptin such as metabolic syndrome.
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Chen, Nan, Zeyu Qiao, and Chu Wang. "A chemoselective reaction between protein N-homocysteinylation and azides catalyzed by heme(ii)." Chemical Communications 55, no. 25 (2019): 3654–57. http://dx.doi.org/10.1039/c9cc00055k.

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Chen, Nan, Jinmin Liu, Zeyu Qiao, Yuan Liu, Yue Yang, Changtao Jiang, Xian Wang, and Chu Wang. "Chemical proteomic profiling of proteinN-homocysteinylation with a thioester probe." Chemical Science 9, no. 10 (2018): 2826–30. http://dx.doi.org/10.1039/c8sc00221e.

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Xu, Leilei, Jiajia Chen, Jun Gao, Hongxiu Yu, and Pengyuan Yang. "Crosstalk of homocysteinylation, methylation and acetylation on histone H3." Analyst 140, no. 9 (2015): 3057–63. http://dx.doi.org/10.1039/c4an02355b.

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Jakubowski, H. "Protein N-homocysteinylation: implications for atherosclerosis." Biomedicine & Pharmacotherapy 55, no. 8 (October 2001): 443–47. http://dx.doi.org/10.1016/s0753-3322(01)00085-3.

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Jakubowski, Hieronim. "Protein N-Homocysteinylation and Colorectal Cancer." Trends in Cancer 5, no. 1 (January 2019): 7–10. http://dx.doi.org/10.1016/j.trecan.2018.10.006.

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Perna, A. F., E. Satta, F. Acanfora, C. Lombardi, D. Ingrosso, and N. G. De Santo. "Increased plasma protein homocysteinylation in hemodialysis patients." Kidney International 69, no. 5 (March 2006): 869–76. http://dx.doi.org/10.1038/sj.ki.5000070.

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Colgan, Stephen M., and Richard C. Austin. "Homocysteinylation of Metallothionein Impairs Intracellular Redox Homeostasis." Arteriosclerosis, Thrombosis, and Vascular Biology 27, no. 1 (January 2007): 8–11. http://dx.doi.org/10.1161/01.atv.0000254151.00086.26.

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Balint, Brittany, Sébastien Hergalant, Jean-Michel Camadro, Sébastien Blaise, Laetitia Vanalderwiert, Laurent Lignières, Rosa-Maria Guéant-Rodriguez, and Jean-Louis Guéant. "Fetal Programming by Methyl Donor Deficiency Produces Pathological Remodeling of the Ascending Aorta." Arteriosclerosis, Thrombosis, and Vascular Biology 41, no. 6 (June 2021): 1928–41. http://dx.doi.org/10.1161/atvbaha.120.315587.

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Objective: Deficiency in vitamin B12/folate (methyl donor deficiency [MDD]) produces cardiovascular outcomes during aging and fetal programming effects in newborns of MDD mothers. Whether fetal programming provokes long-term effects on aorta remains largely unknown. Approach and Results: We investigated the impact of fetal programming on ascending aorta of aged rats born from mothers subjected to MDD during gestation/lactation. We performed morphological and molecular examinations of ascending aortas in 21 days- and 400 days-aged rats with initial MDD fetal programming (iMDD) compared with control matched rats. iMDD induces remodeling of the ascending aorta in aged rats, with collagen deposition ( P =0.0008), decreased thickness of elastin ( P <0.0001), and 8.7-fold increase of elastin breaks ( P =0.0002). Proteomic analyses, Western blotting, and immunohistochemical examination revealed decreased expression of α-smooth muscle actin, vinculin, SM22α (smooth muscle 22α), and N-cadherin and increased expression of TGF (transforming growth factor) β1. Elastin breaks were correlated to increased neutrophil elastase ( P =0.0002), cathepsin-K ( P =0.0002), cathepsin-S ( P <0.0001), MMP (matrix metalloproteinase) 9, and MMP2 ( P <0.0001 and P =0.02). Proximity Duolink ligation assay showed homocysteinylation of actin-associated and extracellular matrix proteins, including SM22α ( P =0.01), N-cadherin ( P =0.0008), and vinculin ( P =0.001), which was associated with elastin breaks ( P =0.002) and increased expression of MARS (methionyl-tRNA synthetase; involved in irreversible protein homocysteinylation). Furthermore, we observed an inverse relationship between elastin breaks and blood pressure (systolic, P =0.004 and diastolic, P =0.0007). Conclusions: MDD fetal programming produced altered integrity and remodeling of ascending aorta during aging and irreversible MARS-associated homocysteinylation of key proteins of extracellular matrix and elastin homeostasis. This contributes to understanding why homocysteine-lowering vitamin B supplementation fails to relieve vascular complications in adulthood.
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Jamroz-Wiśniewska, A., J. Bełtowski, H. Bartosik-Psujek, G. Wójcicka, and K. Rejdak. "Processes of plasma proteinN-homocysteinylation in multiple sclerosis." International Journal of Neuroscience 127, no. 8 (October 14, 2016): 709–15. http://dx.doi.org/10.1080/00207454.2016.1241782.

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Dissertations / Theses on the topic "Homocysteinylation"

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Lemos, Ana Rita Marques. "Molecular targeting of proteins by homocysteine: implications in familial and clinical hypercholesterolemia." Master's thesis, 2015. http://hdl.handle.net/10362/16330.

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Cardiovascular diseases (CVDs) are one of the leading causes of death and disability worldwide and one of its underlying causes is hypercholesterolemia. Hypercholesterolemia can have genetic (familial hypercholesterolemia, FH) and non-genetic causes (clinical hypercholesterolemia, CH), the first much more severe, with occurrence of premature atherosclerosis. While the pathophysiological role of homocysteine (Hcy) on CVD is still controversial, molecular targeting of protein by S and N-homocysteinylation offers a new paradigm to be considered in the vascular pathogenesis of hypercholesterolemia. On this regard, the present study aims to give new insights on protein targeting by Hcy in both CH and FH conditions. A total of 187 subjects were included: 65 normolipidemic and 122 hypercholesterolemic. Total (tHcy) and free (fHcy) fractions were quantified in serum samples after validation of an HPLCFD method, to assess S-homocysteinylation. Also, the lactonase (LACase) activity of paraoxonase-1 (PON1) was quantified by a colorimetric assay, as a surrogate of N-homocysteinylation. tHcy does not differ among groups. Nevertheless, fHcy declines in the hypercholesterolemic groups, with more evidence to the FH population. Consequently, there seems to be an increase of Shomocysteinylation, regardless of lipid lowering therapy (LLT). Also, despite of LLT use, LACase activity is lower in FH, thus the risk for protein N-homocysteinylation seems to be higher. Moreover, the decrease in LACase/ApoA1 and LACase/HDL ratios in FH, shows that HDL is dysfunctional in this population, despite its normal concentration values. Data supports that the pathophysiological role of Hcy on hypercholesterolemia may reside in its ability to post-translationally modify proteins. This role is particularly evident in FH condition. In the future, it will be interesting to identify which target proteins are modified and thus involved in vascular pathology progression.
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Book chapters on the topic "Homocysteinylation"

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Jakubowski, Hieronim. "Pathophysiological Consequences of Protein N-Homocysteinylation." In Homocysteine in Protein Structure/Function and Human Disease, 107–19. Vienna: Springer Vienna, 2013. http://dx.doi.org/10.1007/978-3-7091-1410-0_6.

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Jakubowski, Hieronim. "Discoveries of Protein S- and N-Homocysteinylation." In Homocysteine in Protein Structure/Function and Human Disease, 55–57. Vienna: Springer Vienna, 2013. http://dx.doi.org/10.1007/978-3-7091-1410-0_4.

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