PARK7 Antibody
- Known as:
- PARK7 Antibody
- Catalog number:
- 32112
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- PARK7 Antibody
Related genes to: PARK7 Antibody
- Gene:
- PARK7 NIH gene
- Name:
- Parkinsonism associated deglycase
- Previous symbol:
- -
- Synonyms:
- DJ-1, DJ1, GATD2
- Chromosome:
- 1p36.23
- Locus Type:
- gene with protein product
- Date approved:
- 2001-08-07
- Date modifiied:
- 2018-07-11
Related products to: PARK7 Antibody
Related articles to: PARK7 Antibody
- According to the Global Burden of Disease Study 2023, Parkinson's disease (PD) affects an estimated 11.67 million people worldwide, a progressive neurodegenerative condition marked by the accumulation of Lewy bodies containing α-synuclein and the progressive loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Over the past ten years, advances in genetic and molecular research have shown that PD pathogenesis involves interrelated mechanisms such as impaired protein homeostasis, mitochondrial dysfunction, oxidative stress, defects in lysosomal-autophagic pathways, and chronic neuroinflammation, which go beyond dopaminergic neuronal loss. This review summarizes new data about major genes associated with monogenic and polygenic forms of PD, including SNCA, LRRK2, PRKN, PINK1, DJ-1 (PARK7), GBA1, VPS35, ATP13A2, FBXO7, and the GWAS-prioritized risk genes TMEM175, SCARB2, CTSB, RIT2, DYRK1A, and BAG3, together with the molecular pathways disrupted by these genetic alterations in light of current evidence. The polygenic architecture of PD and ancestry-related variation in genetic risk are also discussed. α-synuclein aggregation and proteostasis networks, oxidative stress, autophagy and mitophagy failure, neuroinflammation, mitochondrial quality control, and epigenetic regulation are all given special attention. Apart from traditional dopaminergic treatments, new therapeutic approaches such as immunotherapies targeting α-synuclein, gene therapies mediated by adeno-associated virus (AAV), induced pluripotent stem cell (iPSC)-based methods, and genotype-guided precision medicine are critically examined. A more comprehensive understanding of the molecular mechanisms underlying PD is expected to facilitate the development of reliable biomarkers and accelerate the clinical translation of disease-modifying therapies. - Source: PubMed
Publication date: 2026/09/28
Yildirim Sumeyye - Tarin exhibits immunomodulatory and antiproliferative properties against several tumor cell lines. Nano-encapsulation in liposomes enhances its therapeutic potential by improving protein stability, bioavailability, and sustained release. Previous studies demonstrated that nano-encapsulated tarin induces cell cycle arrest, migration inhibition, apoptosis, and autophagy in triple-negative breast cancer cells; however, the molecular mechanisms underlying these effects remain poorly understood. To investigate the proteomic response elicited by nano-encapsulated tarin, MDA-MB-231 cells were treated for 24 and 48 h. Intracellular proteins were extracted, digested with trypsin, and analyzed by label-free LC-2D-MS/MS using HDMSE acquisition. Differentially expressed proteins were identified and quantified using the Progenesis QI platform, and then functional classification and pathway enrichment analyses were performed. A total of 2818 proteins were identified, of which 2150 displayed time-dependent modulation following treatment. After 24 h, cells exhibited an adaptive stress response profile characterized by increased DNA repair proteins (, ), migration/remodeling factors (, , ), and immune/cell cycle regulators (, ), while antioxidant proteins (, ) and BRCA1 were reduced, indicating oxidative stress and DNA damage. After 48 h, the proteomic profile shifted toward cell death, with increased , , , and CASP8 expression, disruption of DNA repair and cell cycle regulators (, , , ), and decreased migration-related proteins (, , , ). Nano-encapsulated tarin promotes a time-dependent transition from early adaptive stress responses to apoptosis, autophagy, cell cycle disruption, and loss of migratory capacity. These findings provide novel insights into the molecular mechanisms underlying tarin antitumoral activity and support its potential as a promising therapeutic strategy against triple-negative breast cancer. - Source: PubMed
Publication date: 2026/09/07
Cardoso Raiane VPereira Patricia RFreitas Cyntia SSouza Yuri PKalume Dário EVerissimo da Costa Giovani CarloConte-Junior Carlos APaschoalin Vania Margaret Flosi - Alzheimer's disease (AD) is a gradual neurodegenerative disorder presenting with cognitive and non-cognitive impairment. Currently approved therapies alleviate symptoms but do not modify disease progression and may be associated with adverse effects. - Source: PubMed
Publication date: 2026/09/20
Kumar AnuragFatima NasreenKumar PramodNath RajendraSachan Amod KumarDixit Rakesh KumarPal Rishi - Parkinson's disease (PD) is a progressive neurodegenerative disorder primarily affecting dopaminergic neurons in the mesencephalon. With rising global incidence, especially in individuals over 60, PD presents with motor and non-motor symptoms. While monogenic forms account for a subset of cases, genetic heterogeneity and variable expressivity complicate diagnosis and management. This study aimed to evaluate the genetic profile of a Turkish PD cohort through clinical exome sequencing (CES), assess genotype-phenotype correlations, and identify structural rearrangements. A retrospective analysis was conducted on 137 patients diagnosed with Parkinson's disease according to the Movement Disorder Society (MDS) clinical diagnostic criteria. Targeted next-generation sequencing (NGS) analysis was performed, and identified genetic variants were strictly classified in accordance with the American College of Medical Genetics and Genomics (ACMG) guidelines and current gene-disease validity consensus. Copy number variations (CNVs) were assessed utilizing NGS read-depth algorithms. Following rigorous evaluation according to ACMG criteria and current gene-disease validity consensus, definitive disease-causing variants explaining the PD phenotype were identified in 10 patients (7.30%). This definitive diagnostic yield was driven entirely by established PD loci: GBA1 (9 patients) and a homozygous deletion in PRKN (1 patient). Beyond this definitive group, several notable variants in OMIM-associated PD genes (including LRRK2, FBXO7, PARK7, and EIF4G1) were characterized as VUS or susceptibility findings, displaying strong clinical correlations with progressive motor and complex phenotypes. A monoallelic PINK1 variant and findings in GIGYF2 and UCHL1 were strictly excluded from the causal diagnostic yield. A novel heterozygous duplication involving LRRK2 exons 6-20 was also identified; however, as it likely results in a loss of function, its pathogenicity remains uncertain under dominant gain-of-function models. Clinical exome sequencing effectively delineates the complex genetic landscape of PD in the Turkish population. While the definitive diagnostic rate is 7.30% under strict causal criteria, the characterization of prominent VUS in OMIM-associated genes and a novel LRRK2 structural variant undetected by routine MLPA highlights the evolving complexity of PD genetics and the critical need for integrating comprehensive, read-depth-based CNV analysis into standard pipelines. - Source: PubMed
Publication date: 2026/09/19
Canbek SezinGulseven M FatihMert GoncagulSenol M Guney - A persistent barrier to optimizing the utilization of deceased donor kidneys, nearly 30% of which are discarded, is the absence of objective, molecularly resolved metrics of organ quality. To address this gap, we integrated high-resolution proteoform imaging mass spectrometry (PiMS) of donor kidney biopsies with deep LC-MS-based intact proteoform profiling of recipient peripheral blood mononuclear cells (PBMCs) and standard clinical assays. This approach enables direct delineation of proteoform landscapes and reveals immunological and cell stress signatures. Across donor types, living donor (LD) kidneys were enriched for proteoforms associated with oxidative metabolism and cellular homeostasis, whereas kidneys from donation after brain death (DBD), donation after circulatory death (DCD), and discarded organs exhibited elevated abundance of stress-responsive proteoforms, including acetylated CRYAB, PARK7, S100A4, and ACTG1. Despite more pronounced early allograft dysfunction in DCD recipients, DCD tissue proteoform landscapes were globally more similar to LD than to DBD kidneys, indicating distinct injury biology not captured by clinical metrics or peptide-centric proteomics. To extend these findings beyond the graft, we performed the first paired tissue and PBMC proteoform profiling across donor types. Baseline PBMC proteoform differences were minimal; however, by day 7 post-transplant, recipients of deceased donor kidneys exhibited platelet activation, cytoskeletal stress, and inflammatory signaling. Several PBMC-derived proteoforms correlated with serum creatinine, highlighting their potential as early, objective indicators of graft adaptation. Collectively, this proof-of-concept study defines conserved injury-associated proteoforms across tissue and immune compartments and support the idea that proteoform-resolved analysis may provide a mechanistically grounded, objective framework for assessing donor kidney quality and early graft function. - Source: PubMed
Publication date: 2026/09/18
Ctortecka ClaudiaJaishankar DineshSu PeiHuang Che-FanPla IndiraHenning NathanielHollas Michael A RCallegari Michelle ATaylor Meredith ELee Yu MinDaud AmnaPinelli David FRohan VinayakCaldwell Michael AForte EleonoraSanchez AnielKelleher Neil LNadig Satish N