Ask about this productRelated genes to: DUSP10 antibody
- Gene:
- DUSP10 NIH gene
- Name:
- dual specificity phosphatase 10
- Previous symbol:
- -
- Synonyms:
- MKP-5, MKP5
- Chromosome:
- 1q41
- Locus Type:
- gene with protein product
- Date approved:
- 1999-11-26
- Date modifiied:
- 2015-09-11
Related products to: DUSP10 antibody
Related articles to: DUSP10 antibody
- Progressive supranuclear palsy (PSP) is a tauopathy and has a multifactorial etiology. The genetic component comprises at least 15 genes with unrelated functions that increase risk for PSP with a high degree of certainty. The function of these genes in increasing risk for PSP is presently unknown. This study was undertaken to identify new pathological pathways of these genes/proteins in increasing risk for PSP. Identification of possible targets and pathways of these genes was investigated using publicly available databases. 13 out of 15 of the risk genes, i.e. , and target microtubules, and directly alter their function via variable mechanisms. We now present data that these pathways are predicted to involve common pathways strongly involving microtubule hemeostasis, such as vesicle transport of misfolded proteins to lysosomes and cellular export. Two genes ( and ) are not obviously directly targeting microtubules. Mutations of the risk genes interfere with microtubular function and/or structure as they relate to axon formation/integrity, axon transport, intracellular organelle transport and communication, and cellular, microtubule - guided waste management. Microtubules may be thought of as a conveyor belt for the distribution of nutrients and waste management. Taken together these alterations include an increased risk of tau precipitation (MAPT) and are molecular drivers of neuronal degeneration in PSP. Although microtubular dysfunction has long been documented in PSP mainly based on the findings related to MAPT, this is the first study of the effect of risk genes in PSP. We demonstrate that most of these genes (13/15) also affect microtubular structure and function. These genes/proteins may also be biased towards neurodegeneration in motor neurons. - Source: PubMed
Publication date: 2026/04/20
Donlon Timothy AMüller Ulrich - Glioblastoma multiforme is an aggressive and therapy-resistant tumor, necessitating the identification of novel therapeutic targets. Here, we investigated the role of transient receptor potential vanilloid 1 (TRPV1) in mediating capsaicin-induced changes in cell viability in U87 glioblastoma cells. Wild-type cells tolerated capsaicin concentrations up to 175 μM, whereas TRPV1 knockout (TRPV1KO) cells exhibited reduced viability at 164 μM, indicating a cytoprotective function of TRPV1. Transcriptomic analyses revealed that wild-type cells activated the MAPK-MSTRG.66879-MYC-HSF1-axis, resulting in robust induction of heat shock proteins (HSPA1B, HSPA6, HSP90AA1) and dual-specificity phosphatases (DUSP1, DUSP8, DUSP10), which collectively maintained protein homeostasis and mitigated cellular damage. In contrast, TRPV1KO cells displayed impaired calcium-mediated MAPK activation, leading to altered mitochondrial oxidative phosphorylation, significant changes in electron transport chain (ETC I, II, III, IV), and enhanced intrinsic apoptosis through HRK. Notably, two long non-coding RNAs, MSTRG.56099 and MSTRG.66879, were identified as potential cis-regulators of DUSP1 and MYC, respectively. MSTRG.66879, upregulated in wild-type cells, appeared to form a TRPV1-associated regulatory axis with MYC and miR-182, promoting cell survival under capsaicin exposure. Disruption of this network in TRPV1KO cells sensitized them to capsaicin-induced apoptosis. Collectively, TRPV1 orchestrates calcium influx, MAPK signaling, heat shock protein induction, and noncoding RNA-mediated regulation to facilitate glioblastoma cell adaptation, suggesting that targeting TRPV1 and the MSTRG.66879-MYC axis may offer new therapeutic avenues and biomarkers for glioblastoma management. - Source: PubMed
Publication date: 2026/04/10
Chinreddy Subramanyam ReddyMashozhera Nicole TendayiLee GwonjinZaman IqraaPatel VaibhaviHarris Robert THankins Gerald RReddy Umesh K - To investigate the protective effects and underlying mechanisms of tanshinone IIA in preventing septicemia acute kidney injury (SA-AKI). - Source: PubMed
Publication date: 2026/01/15
Wen DanDeng QingZeng YingLi LongzhuYang XinChen QinkaiYan YanLv Jinlei - The family Cyprinidae is predominantly restricted to freshwater habitats, making the evolution of diadromy and seawater adaptation exceptionally rare within this group. , a rare anadromous cyprinid, and its strictly freshwater congener , provide an ideal comparative model to investigate the molecular mechanisms underlying salinity adaptation. This study aimed to elucidate the tissue-specific transcriptional reprogramming, identify candidate genes and key pathways, and explore their association with seawater acclimation in . - Source: PubMed
Publication date: 2026/01/09
Xu ZiyueZheng WenChen WenjunZhou MinZhai DongdongXia MingLiu HongyanXiong FeiWang Ying - Therapeutic application of ex vivo expanded regulatory T cells is a promising approach to prolong allograft survival. In this work we performed a detailed characterization of a preclinical heterogenous antigen specific T enriched regulatory cell line (ASTRL) expanded ex vivo from PBMC of stable kidney transplant recipients. We used three different approaches: scRNA-seq, flow cytometry and mass cytometry, to compare pre-expansion PBMC to post-expansion ASTRL. Results show the CD4 T cell compartment in ASTRL clonally expanded in response to donor antigen stimulation and showed decreased TCR diversity. ASTRL CD4 T cells demonstrated a Treg associated transcriptome with upregulated CD39 and TIGIT together with other classical Treg genes like IL2RA, IKZF4, TNFRSF9, CXCR6, DUSP10 and HLA-DRA. Comparison of differentially expressed genes (DEGs) in ASTRL with classical Treg gene signatures showed strong overlap of genes associated with both peripheral and uterine Tregs together with a Th2-like Treg transcriptomic profile. In conclusion the CD4 T cell compartment of ASTRL acquire a regulatory T cell transcriptomic profile in response to donor antigen specific stimulation. This suggests a promising approach towards the development of a regulatory cell therapy in organ transplantation. - Source: PubMed
Publication date: 2026/01/14
Tripathi SudiptaJulé Amélie MZhuo ZhuSchreiber Brittany LMartin-Moreno Paloma LSui Shannan HoWaaga-Gasser Ana MariaChandraker Anil