MGC4618 antibody - N-terminal region (ARP34360_T100)
- Known as:
- MGC4618 (anti-) - N-terminal region (ARP34360_T100)
- Catalog number:
- arp34360_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- MGC4618 antibody - N-terminal region (ARP34360_T100)
Related genes to: MGC4618 antibody - N-terminal region (ARP34360_T100)
- Gene:
- TMEM175 NIH gene
- Name:
- transmembrane protein 175
- Previous symbol:
- -
- Synonyms:
- MGC4618
- Chromosome:
- 4p16.3
- Locus Type:
- gene with protein product
- Date approved:
- 2006-08-29
- Date modifiied:
- 2015-09-29
Related products to: MGC4618 antibody - N-terminal region (ARP34360_T100)
Related articles to: MGC4618 antibody - N-terminal region (ARP34360_T100)
- Gut microbiota dysbiosis contributes to Parkinson's disease (PD) pathology by altering dopamine metabolism in the gut-brain axis. Although probiotics and other functional strains have been proposed as microbiome-based interventions, few naturally occurring gut microbes show therapeutic potential for PD. Here, we isolated Enterococcus hirae QT4713 (QT4713) from the hypoxic, low-pressure Qinghai-Tibet Plateau (4713 m altitude). Whole-genome sequencing revealed that QT4713 harbors a tyrosine decarboxylase gene (TyrDc), enabling conversion of L-tyrosine to dopamine in vitro. In mice, QT4713 enhanced antioxidant enzyme activity, reduced inflammatory mediators, reshaped gut microbial composition, and promoted short-chain fatty acid production. Metabolomic analyses indicated activation of L-tyrosine metabolism, with increased L-DOPA and dopamine levels in the colon and feces, accompanied by improved motor performance. In an MPTP-induced PD mouse model, QT4713 alleviated motor and gastrointestinal dysfunction, reduced oxidative and inflammatory damage, and attenuated dopaminergic neuron loss. QT4713 also increased dopamine and tyrosine levels in the striatum. Extending beyond an acute toxin model, QT4713 partially rescued PD-like phenotypes in TMEM175 knockout mice, preserving tyrosine hydroxylase-positive neurons in the substantia nigra. Together, these findings suggest that QT4713 can mitigate gastrointestinal disturbances and other PD-related deficits, consistent with combined effects on catecholamine-related metabolism and gut microbiota remodeling. - Source: PubMed
Publication date: 2026/05/19
Zhao TingtingLi BinLiu YimingZhang JiaruiFan XueniAo MingyangNiu YuanlinLi DiantongHe JinSun DongWu HuiTang TuoxianLiu ZhenjiangHuang Xiaodan - Current review aims to clarify the role of lysosomal genes in the pathogenesis of Parkinson's Disease (PD), directing on the molecular mechanisms underlying lysosomal dysfunction and its involvement to α-synuclein accumulation. To deliberates PD-related genes including GBA1, LRRK2, VPS35, PRKN, PINK1, TMEM175, ATP13A2, ATP10B, and DJ1, highlighting their contribution in lysosomal damage. It investigates the disorder of lysosomal enzymes such as cathepsins, glucocerebrosidase, galactocerebrosidase, and acid sphingomyelinase, and the consequent impairment of the autophagic-lysosomal pathway, which helps pathological α-synuclein accumulation. Therapeutic approaches targeting lysosomal dysfunction and α-synuclein pathology are reviewed, including pharmacological chaperones, immunization strategies, enzyme replacement therapies, and small-molecule oligomer modulators. While recent clinical trials expose certain limitations, combinatorial treatment strategies show potential to improve therapeutic efficacy. Lysosomal pathways are critical contributors to PD pathogenesis and denote promising targets for intervention. Integrating mechanistic understandings with developing therapies underlines the importance of targeting lysosomal dysfunction to mitigate α-synuclein aggregation and advance PD treatment. - Source: PubMed
Publication date: 2026/05/11
Chand Bala VidhanKumar Gupta AsheeshKumar AmitKumar Singh MukeshKumar Patel ArvindKumar Tiwari SunilKumar Sushil - The precise maintenance of the intra-lysosomal acidic microenvironment is vital for neuronal functions, including protein degradation, metabolic regulation, and organelle quality control. This review systematically elucidates the dynamic regulatory network governing neuronal lysosomal pH homeostasis, transcending the classical proton pump-leak model. We highlight a multifaceted system integrating vacuolar-type H-ATPase (V-ATPase)-driven active proton pumping, proton leakage mediated by channels such as transmembrane protein 175 (TMEM175) and solute carrier family 7 member 11 (SLC7A11), membrane potential buffering by the Cl/H exchanger ClC-7, and regulatory signaling pathways involving AMP-activated protein kinase (AMPK)-mechanistic target of rapamycin complex 1 (mTORC1)-transcription factor EB (TFEB). Crucially, pH dysregulation-manifesting as hyperacidification, alkalinization, or the increasingly recognized and potentially more deleterious phenomenon of dynamic instability-emerges as a fundamental pathogenic mechanism in neurodegenerative disorders like Alzheimer's disease (AD) and Parkinson's disease (PD). Such disruption impairs autophagic flux and mitochondria-lysosome crosstalk, triggering neuroinflammation and ultimately leading to neuronal dysfunction and death. Building upon these mechanistic insights, we discuss emerging therapeutic strategies, advocating a paradigm shift from merely correcting acid-base imbalance toward restoring intrinsic lysosomal pH homeostatic resilience. Finally, we outline critical challenges for clinical translation, including deciphering neuron subtype-specific mechanisms, identifying dynamic in vivo pH biomarkers, and developing brain-penetrant therapeutics. Overcoming these hurdles through interdisciplinary innovation is essential to advance lysosomal pH-targeted therapies into clinical practice. - Source: PubMed
Publication date: 2026/04/17
Tang YifangGuo TaoHe HongyunDeng Yihao - Regional brain atrophy has been observed in dementia with Lewy bodies (DLB), yet determinants of regional vulnerability remain unclear. Using imaging transcriptomics, we examined whether normative gene expression patterns relate to regional atrophy in DLB. We included 164 DLB patients (49 women) and 164 age- and sex-matched healthy controls from three European centres and the Mayo Clinic, USA. Volumetric atrophy was quantified from T1-weighted MRI across 58 left-hemispheric regions using w-scores. Normative expression of twelve genes implicated in alpha-synuclein, beta-amyloid, and tau pathology was extracted from the Allen Human Brain Atlas. DLB patients showed diffuse atrophy across most regions. In the full cohort, normative expression of MAPT, PINK1, and PSEN2 predicted regional atrophy after correction for spatial autocorrelation, although none survived multiple-testing correction. In the Mayo Clinic sub-cohort, expression of APP, BIN1, GBA, MAPT, PINK1, SNCA, and TMEM175 significantly predicted atrophy and survived multiple-testing correction. Random forest models did not outperform spatial null models in the full cohort, but PARK7, PINK1, and PSEN2 consistently emerged as important predictors. A significant global model was observed in the Mayo Clinic sub-cohort, driven by GBA, LRP1, and PINK1. These findings suggest that normative gene expression partially contributes to regional brain atrophy in DLB. - Source: PubMed
Publication date: 2026/04/16
Habich AnnegretBaumann Janna MSchwarz Christopher GPrzybelski Scott AInguanzo AnnaOppedal KetilBlanc FrédéricLemstra Afina WHort JakubBoeve Bradley FAarsland DagWestman EricDierks ThomasKantarci KejalJonkman Laura EFerreira Daniel - - Source: PubMed
Publication date: 2026/04/13
Sun WenhuaSchulte ClaudiaGasser ThomasTan Manuela