MGC4618 antibody - N-terminal region (ARP34360_P050)
- Known as:
- MGC4618 (anti-) - N-terminal region (ARP34360_P050)
- Catalog number:
- arp34360_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- MGC4618 antibody - N-terminal region (ARP34360_P050)
Related genes to: MGC4618 antibody - N-terminal region (ARP34360_P050)
- 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_P050)
Related articles to: MGC4618 antibody - N-terminal region (ARP34360_P050)
- 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 - Chronic pain remains a pervasive and debilitating condition with few effective treatments available. Emerging evidence reveals that transmembrane (TMEM) proteins are not merely passive structural elements but dynamic regulators of nociceptive signaling. Key TMEM family members, including TMEM100, TMEM16A/F, TMEM175, TMEM97, TMEM120A/TACAN, and TMEM233, orchestrate pain transmission by modulating ion channels, inflammatory mediators, and intracellular signaling cascades across peripheral and central pathways. Decoding their structural and functional diversity reveals new opportunities to design targeted analgesics that disrupt pathological pain at its source while sparing central nervous system side effects. By harnessing the therapeutic potential of TMEM proteins, we may redefine strategies for managing chronic and treatment-resistant pain, ultimately improving outcomes for millions affected worldwide. - Source: PubMed
Publication date: 2026/04/10
Deepika KapparaVerma NiveditaTiwari Vinod - Lysosomal dysfunction exacerbates cardiomyocyte damage in myocardial infarction (MI) by impairing cellular degradation. However, the precise molecular mechanisms driving this pathologic process remain unclear. Lysosomal transmembrane protein 175 (TMEM175) is critical for regulating lysosomal homeostasis. But its pathophysiological implications in post-infarction cardiac dysfunction are not fully understood. By using both gain and loss of function approaches in vivo and in vitro, we discovered that TMEM175 overexpression conferred cardioprotection in MI models. This was evidenced by reduced infarct size, collagen deposition, and myocardial injury, accompanied by restored lysosomal function characterized by increased biogenesis, normalized pH, enzyme activities, and autophagic flux. Conversely, TMEM175 knockdown exacerbated these pathologies. Under hypoxic stress, TMEM175 overexpression in neonatal mouse cardiomyocytes (NMCMs) improved cell viability and corrected lysosomal dysfunction, whereas its knockdown worsened the aforementioned effects. Mechanistically, the reduction of TMEM175 induced by MI increases mammalian target of rapamycin complex 1 (mTORC1) phosphorylation on lysosomal membranes and suppresses the nuclear translocation of transcription factor EB (TFEB), thereby impairing TFEB's transcriptional regulation of lysosome-associated genes. Meanwhile, TMEM175 restoration reversing this cascade, and restoring lysosomal function and autophagic flux. - Source: PubMed
Publication date: 2026/02/25
Chen ChenLou HanHu An-GeHuang QiangKong Ling-YiChen Zhou-XiuXu Heng-HuiChen Yong-ChaoLiu HengDuan Shu-QinLin YuanZhao Li-MinLiu LingKhoso Muneer AhmedLiu XinZhang Yong