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Artykuły w czasopismach na temat „DJ-1 Family Protein”

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Data publikacji: 6 września 2023

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1

Lin, Rong-Rong, Qing-Qing Tao, and Zhi-Ying Wu. "Early-Onset Parkinson’s Disease and Brain Iron Accumulation Caused by a Novel Homozygous DJ-1 Mutation." Journal of Parkinson's Disease 12, no. 3 (2022): 813–19. http://dx.doi.org/10.3233/jpd-213033.

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DJ-1 mutations are rare causes of autosomal recessive early-onset Parkinson’s disease (AR-EOPD) and relatively rarely reported in the Chinese population. Here, we used the whole-exome sequencing and Sanger sequencing to investigate DJ-1 mutations in the Chinese population and confirmed the pathogenicity of the mutation using primary fibroblasts established from skin biopsies. We identified a novel homozygous mutation (c.390delA, p.D131Tfs*3) in DJ-1 in a consanguineous Chinese family. The proband in this family had parkinsonism at the age of 22. His brain MRI indicated brain iron accumulation

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Qin, Li-xia, Jie-qiong Tan, Hai-nan Zhang, et al. "BAG5 Interacts with DJ-1 and Inhibits the Neuroprotective Effects of DJ-1 to Combat Mitochondrial Oxidative Damage." Oxidative Medicine and Cellular Longevity 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/5094934.

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Loss-of-function mutations in gene encoding DJ-1 contribute to the pathogenesis of autosomal recessive early-onset familial forms of Parkinson’s disease (PD). DJ-1 is a multifunctional protein and plays a protective role against oxidative stress-induced mitochondrial damage and cell death, but the exact mechanism underlying this is not yet clearly understood. Here, using coimmunoprecipitation (Co-IP) and immunofluorescence methods, we prove that Bcl-2-associated athanogene 5 (BAG5), a BAG family member, interacts with DJ-1 in mammalian cells. Moreover, we show that BAG5 could decrease stabilit

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Lewandowska, Aleksandra, Trung Nghia Vo, Thuy-Dung Ho Nguyen, et al. "Bifunctional Chloroplastic DJ-1B from Arabidopsis thaliana is an Oxidation-Robust Holdase and a Glyoxalase Sensitive to H2O2." Antioxidants 8, no. 1 (2019): 8. http://dx.doi.org/10.3390/antiox8010008.

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Members of the DJ-1 protein family are multifunctional enzymes whose loss increases the susceptibility of the cell to oxidative stress. However, little is known about the function of the plant DJ-1 homologs. Therefore, we analyzed the effect of oxidation on the structure and function of chloroplastic AtDJ-1B and studied the phenotype of T-DNA lines lacking the protein. In vitro oxidation of AtDJ-1B with H2O2 lowers its glyoxalase activity, but has no effect on its holdase chaperone function. Remarkably, upon oxidation, the thermostability of AtDJ-1B increases with no significant alteration of

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4

Kolisek, Martin, Augusto C. Montezano, Gerhard Sponder, et al. "PARK7/DJ-1 dysregulation by oxidative stress leads to magnesium deficiency: implications in degenerative and chronic diseases." Clinical Science 129, no. 12 (2015): 1143–50. http://dx.doi.org/10.1042/cs20150355.

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Disturbed magnesium (Mg2+) homoeostasis and increased levels of OS (oxidative stress) are associated with poor clinical outcomes in patients suffering from neurodegenerative, cardiovascular and metabolic diseases. Data from clinical and animal studies suggest that MD (Mg2+ deficiency) is correlated with increased production of ROS (reactive oxygen species) in cells, but a straightforward causal relationship (including molecular mechanisms) between the two conditions is lacking. The multifactorial protein PARK7/DJ-1 is a major antioxidant protein, playing a key role in cellular redox homoeostas

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5

Melvin, Prasad, Kondalarao Bankapalli, Patrick D’Silva, and P. V. Shivaprasad. "Methylglyoxal detoxification by a DJ-1 family protein provides dual abiotic and biotic stress tolerance in transgenic plants." Plant Molecular Biology 94, no. 4-5 (2017): 381–97. http://dx.doi.org/10.1007/s11103-017-0613-9.

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Ross, O. A., and M. J. Farrer. "Pathophysiology, pleotrophy and paradigm shifts: genetic lessons from Parkinson's disease." Biochemical Society Transactions 33, no. 4 (2005): 586–90. http://dx.doi.org/10.1042/bst0330586.

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PD (Parkinson's disease) is an aetiologically heterogeneous disorder characterized by a clinical phenotype consisting of resting tremor, rigidity and bradykinesia. Motor symptoms are associated with a progressive loss of dopaminergic neurons, with Lewy body inclusions within surviving neurons. Although heritability studies have shown evidence of familial aggregation, twin studies have provided limited support for a genetic aetiology. Nevertheless, classical linkage methods have nominated 11 regions of the genome and pathogenic mutations have been identified in several genes, including α-synucl

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7

Bankapalli, Kondalarao, SreeDivya Saladi, Sahezeel S. Awadia, Arvind Vittal Goswami, Madhuja Samaddar, and Patrick D'Silva. "Robust Glyoxalase activity of Hsp31, a ThiJ/DJ-1/PfpI Family Member Protein, Is Critical for Oxidative Stress Resistance inSaccharomyces cerevisiae." Journal of Biological Chemistry 290, no. 44 (2015): 26491–507. http://dx.doi.org/10.1074/jbc.m115.673624.

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8

Yang, Xinglong, and Yanming Xu. "Mutations in theATP13A2Gene and Parkinsonism: A Preliminary Review." BioMed Research International 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/371256.

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Parkinson’s disease (PD) is a major neurodegenerative disorder for which the etiology and pathogenesis remain as elusive as for Alzheimer's disease. PD appears to be caused by genetic and environmental factors, and pedigree and cohort studies have identified numerous susceptibility genes and loci related to PD. Autosomal recessive mutations in the genesParkin, Pink1, DJ-1, ATP13A2, PLA2G6, andFBXO7have been linked to PD susceptibility. Such mutations inATP13A2, also namedPARK9, were first identified in 2006 in a Chilean family and are associated with a juvenile-onset, levodopa-responsive type

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9

Liu, Tsai-Wei, Chiung-Mei Chen, and Kuo-Hsuan Chang. "Biomarker of Neuroinflammation in Parkinson’s Disease." International Journal of Molecular Sciences 23, no. 8 (2022): 4148. http://dx.doi.org/10.3390/ijms23084148.

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Parkinson’s disease (PD) is caused by abnormal accumulation of α-synuclein in dopaminergic neurons of the substantia nigra, which subsequently causes motor symptoms. Neuroinflammation plays a vital role in the pathogenesis of neurodegeneration in PD. This neuroinflammatory neurodegeneration involves the activation of microglia, upregulation of proinflammatory factors, and gut microbiota. In this review, we summarized the recent findings on detection of PD by using inflammatory biomarkers, such as interleukin (IL)-1β, IL-2, IL-6, IL-10, tumor necrosis factor (TNF)-α; regulated upon activation,

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10

Ohnishi, Y., and S. Horinouchi. "The A-factor regulatory cascade that leads to morphological development and secondary metabolism in Streptomyces." Biofilms 1, no. 4 (2004): 319–28. http://dx.doi.org/10.1017/s1479050504001462.

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A-factor (2-isocapryloyl-3R-hydroxymethyl-γ-butyrolactone) is a chemical signalling molecule, or microbial hormone, that triggers aerial mycelium formation and secondary metabolism in Streptomyces griseus. A-factor pro- duced in a growth-dependent manner switches on the transcription of adpA, encoding a transcriptional activator, by binding to ArpA, the A-factor receptor protein, which has bound to the adpA promoter, and dissociating the bound ArpA from the DNA. AdpA then activates a number of genes of various functions required for morphological development and secondary metabolism, forming a

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11

Golos, Aleksandra, Dorota Jesionek-Kupnicka, Tadeusz Robak, et al. "The Role of the Slit-Robo Family in Adult Patients with Acute Myeloid Leukemia." Blood 126, no. 23 (2015): 3816. http://dx.doi.org/10.1182/blood.v126.23.3816.3816.

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Abstract Introduction: SLIT-ROBO is newly discovered ligand-receptor family of neuronal guidance molecules. Recently, it has been proved that these proteins are involved in both, physiologic and pathologic angiogenesis. In animal models, it was shown both, pro-and antiangiogenic of SLIT-ROBO signaling. Moreover, the interaction of SLIT ligands with their roundabout receptors (ROBO) results in promotion of apoptosis, adhesion and blocking of cell cycle. There is evidence that SLIT-ROBO proteins are involved in pathogenesis of solid tumors, both in angiogenesis dependent and independent way. The

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12

Zheng, Wei, Xiao Han, Bing Han, et al. "LAR Downregulation Protects the Astrocytic U251 and Cocultured SH-SY5Y Cells in a Rotenone-Induced Parkinson’s Disease Cell Model." International Journal of Molecular Sciences 24, no. 13 (2023): 11111. http://dx.doi.org/10.3390/ijms241311111.

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Leukocyte common antigen-related protein tyrosine phosphatase (LAR) is a member of the protein tyrosine phosphatase family that serves as a key regulator of cellular survival. It is also involved in neurodevelopment and brain disorders. This study was designed to investigate the role of LAR in a cell-based model of Parkinson’s disease (PD) in which U251 and SH-SY5Y cells were used as models of astrocytes and dopaminergic neurons, respectively. Cell viability, cell death, cell morphology, protein phosphorylation and expression, ATP levels, reactive oxygen species (ROS) generation, and mitochond

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13

Oduro, Jennifer, Ronald Simon, Natalia Gorbokon, et al. "95 MAGE-A1 protein expression pattern in > 5,000 tumor and healthy tissue samples: Validation of MAGE-A1 as an ideal target for TCR-based cell therapy." Journal for ImmunoTherapy of Cancer 9, Suppl 2 (2021): A104. http://dx.doi.org/10.1136/jitc-2021-sitc2021.095.

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BackgroundCancer testis antigens (CTAs) are considered attractive targets for T cell receptor (TCR)-based cellular therapies as their expression in healthy adults is considered restricted to the immune-privileged testis. However, low-level expression of some CTAs in healthy tissue has been observed, resulting in significant on-target/off-cancer toxicity. Melanoma associated antigen 1 (MAGE-A1) is a member of the MAGE-A CTA family, whose members are known to influence cellular signaling pathways through their E3 ubiquitin ligase-binding MAGE homology domain. MAGE-A proteins are frequently expre

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14

Yabe, Ichiro, Yuka Hamaya, Hiraku Kameda, et al. "ODP285 A Case of Encephalitis and Adrenal Insufficiency in a Patient With Panhypopituitarism After COVID-19 Vaccination." Journal of the Endocrine Society 6, Supplement_1 (2022): A479—A480. http://dx.doi.org/10.1210/jendso/bvac150.996.

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Abstract Background Since COVID-19 vaccination was introduced, various adverse effects have been linked to the vaccines. In patients with hypopituitarism, adrenal insufficiency due to the side reactions including fever of COVID-19 vaccination is concerned. Clinical Case A 33-year woman was on medical therapy including hydrocortisone (HC) for panhypopituitarism arising from surgical treatment of a pituitary adenoma in 2006. She received a COVID-19 vaccination on day X-3. On day X-2, she developed fever in the morning and became unconscious in the evening. She was brought to our hospital by her

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15

Riabov, Vladimir, Qingyu Xu, Nanni Schmitt, et al. "Preclinical Assessment of Alvocidib in Combination with 5-Azacytidine in High-Risk Myelodysplastic Syndromes." Blood 138, Supplement 1 (2021): 4649. http://dx.doi.org/10.1182/blood-2021-150778.

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Abstract Hypomethylating therapy with 5-azacytidine (5-Aza) is a standard-of-care for patients with higher-risk myelodysplastic syndromes (MDS). Response is induced in approximately 50% of 5-Aza treated patients. However, despite robust efficacy in responders, relapse is almost certain. Recently, inhibitors of anti-apoptotic BCL-2 protein family members have shown potent activity against AML and higher-risk MDS in combination with 5-Aza. Alvocidib (Alv), a cyclin-dependent kinase 9 inhibitor and indirect transcriptional repressor of the anti-apoptotic BCL-2 family member MCL-1, has shown anti-

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16

Ryabov, Vladimir, Nanni Schmitt, Qingyu Xu, et al. "Abstract 6257: Mutations in the ASXL1 and ZRSR2 genes are associated with the response to the combination of alvocidib and 5-azacytidine in higher-risk myelodysplastic syndromes." Cancer Research 82, no. 12_Supplement (2022): 6257. http://dx.doi.org/10.1158/1538-7445.am2022-6257.

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Abstract The hypomethylating agent 5-azacytidine (5-Aza) is a standard-of-care for patients with higher-risk myelodysplastic syndromes (MDS). Although an initial response is induced in approximately 50% of 5-Aza treated patients, subsequent relapse is almost certain. Recently, inhibitors of anti-apoptotic BCL-2 protein family members have shown therapeutic potential in acute myeloid leukemia (AML) and higher-risk MDS. Alvocidib (Alv), a CDK9 inhibitor and indirect transcriptional repressor of the anti-apoptotic factor MCL-1, has shown anti-leukemic effects in a phase 1 study of patients with A

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17

Shen, L., Y. Zhang, Z. Honglin та J. H. W. Distler. "POS0476 THE NUCLEAR RECEPTOR TR4 ORCHESTRATES CYTOSKELETAL ORGANIZATION IN A Gα12/ROCK-DEPENDENT MANNER TO PROMOTE MYOFIBROBLAST DIFFERENTIATION AND TISSUE FIBROSIS IN SYSTEMIC SCLEROSIS". Annals of the Rheumatic Diseases 81, Suppl 1 (2022): 492.2–493. http://dx.doi.org/10.1136/annrheumdis-2022-eular.2033.

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BackgroundNuclear receptors (NR) are a family of transcription factors. Several members of the NR family are candidates for targeted intervention in inflammatory and fibrotic diseases (1-2). Testicular receptor 4 (TR4), also known as Nr2c2, has been shown to regulate fundamental cellular processes such as differentiation, proliferation and growth factor signaling (3-4). However, its role in fibrotic diseases has not been investigated so far.ObjectivesThe aim of the present study was to characterize the role of TR4 in the pathogenesis of fibrotic tissue remodeling in SSc and to interrogate its

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18

Im, Eunju, Lang Yoo, Minju Hyun, Woo Hyun Shin, and Kwang Chul Chung. "Covalent ISG15 conjugation positively regulates the ubiquitin E3 ligase activity of parkin." Open Biology 6, no. 8 (2016): 160193. http://dx.doi.org/10.1098/rsob.160193.

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Parkinson's disease (PD) is characterized by selective loss of dopaminergic neurons in the pars compacta of the substantia nigra and accumulation of ubiquitinated proteins in aggregates called Lewy bodies. Several mutated genes have been found in familial PD patients, including SNCA (α-synuclein), PARK2 (parkin), PINK1 , PARK7 (DJ-1), LRRK2 and ATP13A2 . Many pathogenic mutations of PARK2 , which encodes the ubiquitin E3 ligase parkin, result in loss of function, leading to accumulation of parkin substrates and consequently contributing to dopaminergic cell death. ISG15 is a member of the ubiq

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19

Gupta, Manish K., Puneet Kaur Randhawa, and Michal M. Masternak. "Role of BAG5 in Protein Quality Control: Double-Edged Sword?" Frontiers in Aging 3 (March 3, 2022). http://dx.doi.org/10.3389/fragi.2022.844168.

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Cardiovascular disorder is the major health burden and cause of death among individuals worldwide. As the cardiomyocytes lack the ability for self-renewal, it is utmost necessary to surveil the protein quality in the cells. The Bcl-2 associated anthanogene protein (BAG) family and molecular chaperones (HSP70, HSP90) actively participate in maintaining cellular protein quality control (PQC) to limit cellular dysfunction in the cells. The BAG family contains a unique BAG domain which facilitates their interaction with the ATPase domain of the heat shock protein 70 (HSP70) to assist in protein fo

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20

Weng, Huidan, Wenjing Song, Kangyue Fu, et al. "Proteomic profiling reveals the potential mechanisms and regulatory targets of sirtuin 4 in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson’s mouse model." Frontiers in Neuroscience 16 (January 25, 2023). http://dx.doi.org/10.3389/fnins.2022.1035444.

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IntroductionParkinson’s disease (PD), as a common neurodegenerative disease, currently has no effective therapeutic approaches to delay or stop its progression. There is an urgent need to further define its pathogenesis and develop new therapeutic targets. An increasing number of studies have shown that members of the sirtuin (SIRT) family are differentially involved in neurodegenerative diseases, indicating their potential to serve as targets in therapeutic strategies. Mitochondrial SIRT4 possesses multiple enzymatic activities, such as deacetylase, ADP ribosyltransferase, lipoamidase, and de

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