MCP_HUMAN MIC10 ELISA tesk kit
- Known as:
- MCP_HUMAN MIC10 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen16405
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- MCP_HUMAN MIC10 ELISA tesk kit
Related genes to: MCP_HUMAN MIC10 ELISA tesk kit
- Gene:
- CD46 NIH gene
- Name:
- CD46 molecule
- Previous symbol:
- MIC10, MCP
- Synonyms:
- TRA2.10, MGC26544, TLX
- Chromosome:
- 1q32.2
- Locus Type:
- gene with protein product
- Date approved:
- 1988-08-31
- Date modifiied:
- 2019-04-23
Related products to: MCP_HUMAN MIC10 ELISA tesk kit
Related articles to: MCP_HUMAN MIC10 ELISA tesk kit
- , the etiological agent of Chagas disease, faces profound nutritional and redox stress throughout its life cycle, requiring exceptional metabolic plasticity for survival across insect and mammalian hosts. Despite this, several parasite-specific metabolic pathways remain poorly characterized. Pyrroloquinoline quinone (PQQ)-dependent dehydrogenases are widespread in prokaryotes, where they play crucial roles in the oxidation of various alcohols and sugars. In contrast, their presence in pathogen eukaryotes has remained uncharacterized. Here, we report that the protein Tc323 from is a PQQ-dependent oxidoreductase with conserved structural features and an expanded domain architecture. Computational structural modeling predicted that Tc323 harbors six β-propeller domains, each composed of nine blades, while phylogenetic analyses suggested that this multi-domain architecture originated before the divergence of Trypanosomatidae. Consistent with these predictions, docking simulations revealed high-affinity binding of the PQQ cofactor to all six β-propeller domains, and immunoaffinity-purified Tc323 displayed PQQ-dependent oxidoreductase activity . Localization studies further showed that Tc323 is a membrane-associated protein that localizes to both the endoplasmic reticulum and glycosomes throughout the parasite life cycle and is also released in extracellular vesicles. Together, these findings uncover a previously unrecognized PQQ-dependent activity in and suggest a novel redox-related enzymatic function that may contribute to parasite adaptation to nutritional and oxidative stress. - Source: PubMed
Publication date: 2026/07/07
Gallardo Juan PabloLapadula Walter JesúsOssowski Micaela SoledadNiemirowicz Gabriela TeresaJuri Ayub MaximilianoGómez Karina AndreaPotenza Mariana - The temporal sequence of metabolic conditioning in relation to stress exposure is a fundamental yet underexplored determinant of cellular resilience. Using Saccharomyces cerevisiae as a model, pre-fermentation (50-min fermentation before freezing; FT-50), interrupted fermentation (20-min pre-fermentation before freezing +30-min post-thaw fermentation; FT-20), and post-freezing fermentation (no pre-fermentation, 50-min fermentation after thawing; FT-0) were compared to demonstrate whether pre-fermentation timing dictates freeze-thaw tolerance by reprogramming carbon and redox metabolism. The results showed that a 20-min interrupted fermentation (FT-20) preserves membrane integrity and intracellular pH, sustains pyruvate kinase and catalase activities, and maintains GPX2 expression, thereby limiting oxidative damage. In contrast, post-freezing fermentation triggers futile protectant accumulation and catastrophic membrane disintegration, while continuous pre-fermentation provokes protein complexes collapse. Crucially, we uncover pervasive transcriptional-enzymatic uncoupling: enzyme activities at central metabolic nodes collapse despite massive gene induction, demonstrating that post-translational control-oxidative inactivation and cofactor limitation-serves as the ultimate arbiter of functional competence. The optimal protocol achieves economical resource allocation through moderate trehalose synthesis, sustained glycolytic flux, and preserved NADPH regeneration, avoiding wasteful catabolic cycles. These findings establish a temporal conditioning framework for engineering stress tolerance, with implications spanning industrial fermentation, probiotic cryopreservation, and cell-based therapeutic storage. - Source: PubMed
Publication date: 2026/07/15
Xie DongdongLi XingZheng JiaxinZhao Liang - The biological functions and mechanisms of many cell-type-specific transcriptional cofactors remain unclear. We previously identified () as a repressive transcriptional co-factor that suppresses Crx-mediated transactivation of photoreceptor genes; however, the biological function of remains unclarified. Here, we investigated the functions of and its paralog, (), in mice of either sex. Single knockout (KO) mouse retinas of or did not show significant alterations at both histological and functional levels compared to those of control mice. We then established and examined and double knockout ( DKO) mice. DKO mice exhibited decreased light-evoked activities detected by electroretinogram (ERG), impaired cone photoreceptor morphology revealed by immunohistochemistry, and structural deformity of cone outer segments and synaptic terminals indicated by transmission electron microscopy (TEM), followed by cone death at a later stage. Lipidomics analysis revealed elevated ganglioside levels in DKO retinas, consistent with the increased immunoreactivity of GT1b and GD3 in the outer segment layer. RNA-seq analysis was conducted in a cone-enriched context resulting from deficiency and showed that the gene, whose mutations in humans cause retinitis pigmentosa (RP26), was upregulated in triple KO mice. Transcriptional assays showed that PPL suppressed Crx-mediated transactivation of In addition, AAV-mediated overexpression in the mouse retina induced significant photoreceptor cell death. Taken together, these findings suggest that the repressive Panky and Panky-like co-factors, which modulate Crx transcriptional activities and thus ganglioside levels in the mouse retina, are essential for cone photoreceptor structure and maintenance. The retina is a light-sensing neural tissue in the eye. Photoreceptor cells (PRs) in the retina receive light stimuli. Rod PRs mediate dim-light vision, whereas cone PRs are responsible for bright and color vision. The present study identified that and genes are predominantly expressed in PRs in the mouse retina. and double-knockout mice exhibit impaired cone cell morphology, cone cell death, and visual dysfunction. In addition, gangliosides, which are chemically bonded lipids and sugars essential for cell membrane stability and function, accumulate in the photoreceptor layer. This study showed that and genes regulate ganglioside levels in the retina and play essential roles in the structure and maintenance of cone photoreceptor cells. - Source: PubMed
Publication date: 2026/07/16
Tu Hung-YaGyoten DaichiSumihiro HitoshiMichikawa KayokoMiyanohara YukiHuang ShangyuanAbe ShinyaFujieda KazukiKajimura NaokoChaya TaroIkeda KazutakaFurukawa Takahisa - The misfolding and aggregation of α-synuclein (α-syn), an abundant synaptic protein, leads to the pathogenesis of Parkinson's disease and related synucleinopathies. The cell-to-cell propagation of seeding-competent α-syn is initiated by unconventional protein secretion, yet the physiological pathway(s) underlying this process remain poorly defined. Here we show that α-syn secretion in human cells is mediated by Reticulon-3L (RTN3L)-dependent endoplasmic reticulum autophagy (ER-phagy), a conserved protein quality-control pathway that safeguards ER protein homeostasis. We also demonstrate that RTN3L cooperates with several autophagy regulators, including the ULK1 cofactor FIP200, to drive the delivery of α-syn into an acidic endolysosomal compartment. Increasing concentrations of α-syn disrupt ER-lysosome traffic and α-syn-containing vesicles appear to be rerouted to the cell surface. Consistent with this proposal, knockdown of vesicle associated SNAREs, that mediate fusion at the cell surface, disrupt α-syn secretion. These findings suggest that pathogenic α-syn secretion arises as a by-product of a physiological clearance mechanism, driven by the fusion of autophagosome-derived vesicles with the plasma membrane. Our results provide a conceptual framework for understanding how an intracellular proteostasis pathway, when mis-regulated, could contribute to the spread of neurodegenerative pathology. - Source: PubMed
Publication date: 2026/07/15
Ye YihongKumar KamalXu YueXu FenfenFerro-Novick Susan - In cyanobacteria, the free-living ancestors of chloroplasts, photosynthesis simultaneously sustains growth and generates reactive oxygen species (ROS) that damage proteins, lipids, and DNA when light capture outpaces carbon fixation. Maintaining redox balance, therefore, requires cells to read photosynthetic electron flow as a signal that continuously tunes gene expression and protein activity. This review traces how these redox signals are transduced to transcription machinery through three routes: membrane-localized sensors, cytoplasmic redox sensors downstream of photosystem I, and ROS generated when electron sinks are saturated. Membrane-bound histidine kinases (two-component systems) relay the redox state of the plastoquinone pool to control photosystem remodeling, pigment biosynthesis, and circadian timing. Cytoplasmic one-component regulators, by contrast, sense redox directly through thiol-disulfide switches, iron-sulfur clusters, and metal-catalyzed oxidation to control photosystem-cofactor, electron-carrier, and transition-metal homeostasis. Because many of these regulators persist in algal and plant chloroplasts, cyanobacteria illuminate principles of redox control across photosynthetic eukaryotes. Post-transcriptional and translational control further shapes redox-dependent gene expression programs through transcript stability, ribosome assembly, and translation initiation, extending redox regulation beyond transcription to every step of protein synthesis and even activity modulation. Finally, we connect redox regulation to photosynthetic physiology, stress resilience, and the rational engineering of cyanobacteria for sustainable bioproduction. - Source: PubMed
Publication date: 2026/07/15
Johnson ZacharyYang BinBohutskyi Pavlo