STK4 Mouse Monoclonal Antibody
- Known as:
- STK4 Mouse Monoclonal Antibody
- Catalog number:
- ENZ-006789-M01
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- STK4 Mouse Monoclonal Antibody
Related genes to: STK4 Mouse Monoclonal Antibody
- Gene:
- STK4 NIH gene
- Name:
- serine/threonine kinase 4
- Previous symbol:
- -
- Synonyms:
- MST1, KRS2, YSK3
- Chromosome:
- 20q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-09
- Date modifiied:
- 2019-04-23
Related products to: STK4 Mouse Monoclonal Antibody
Related articles to: STK4 Mouse Monoclonal Antibody
- Metabolic dysfunction-associated steatohepatitis (MASH) is characterized by disrupted hepatic lipid homeostasis and progressive liver injury, and frequently coexists with hypertension and systemic vascular remodeling, suggesting shared pathophysiological mechanisms. Although adipose tissue-derived microRNAs have emerged as important mediators of inter-organ communication, their roles in regulating hepatic cholesterol metabolism and vascular dysfunction during MASH remain incompletely understood. - Source: PubMed
Publication date: 2026/09/02
Xu YuZhang SihanWang KunZhang ChengleiLi JiaruiLi JianningWang LijuanLi Yan - Diabetic cardiomyopathy (DCM) is driven by oxidative stress and an imbalance between autophagy and apoptosis. To improve myocardial delivery of dimethyl fumarate (DMF), a known NRF2-activating redox modulator, and evaluate its association with Mst1 pathway regulation, we developed a cardiac-targeting peptide (APT)-modified biomimetic, reactive oxygen species (ROS)-responsive nanoplatform (NP-APT). NP-APT comprises a ROS-sensitive core and a lipid-cell membrane hybrid coating modified with APT to achieve targeted delivery. The designed nanoplatform demonstrated favorable physicochemical properties, serum/storage stability, macrophage-avoidance capability, and ROS-responsive drug release. In vitro, NP-APT enhanced cardiomyocyte uptake, mitigated high-glucose-induced oxidative stress, restored mitochondrial function and bioenergetic activity, and attenuated apoptosis. Mechanistically, NP-APT protected cardiomyocytes in association with reduced Mst1-related protein abundance, improved autophagy-related signaling, and rebalanced the autophagy-apoptosis equilibrium; Mst1 overexpression weakened these effects, whereas autophagy blockade reduced NP-APT-mediated protection. In a murine DCM model, NP-APT achieved cardiac-specific accumulation, significantly improved cardiac function and fibrosis, and restored cellular homeostasis, with efficacy associated with Mst1 pathway modulation. Hematological, biochemical, behavioral, and histological safety assessments indicated that NP-APT did not produce evident additional systemic toxicity under the tested treatment conditions in DCM mice. Collectively, this study demonstrates that APT-mediated biomimetic nanodelivery provides an effective strategy to enhance DMF myocardial delivery and ameliorate DCM in association with Mst1-autophagy-apoptosis pathway regulation. - Source: PubMed
Publication date: 2026/08/13
Li XinkeLi GuangweiMeng NanaXu WensiTang RunboChen JianqiangWang LuluWang Jun - We report a 6-month-old male, born to consanguineous parents, presented with recurrent bronchopneumonia, global developmental delay, and craniofacial dysmorphism. Initial workup revealed profound T-cell lymphopenia and hypoplasia of the splenium of the corpus callosum. Whole exome sequencing (WES) identified two homozygous pathogenic variants: a mutation in , diagnostic of Temtamy syndrome, and a mutation in , confirming a primary immunodeficiency. At age 3, the patient developed a life-threatening acute hemolytic crisis with a hemoglobin nadir of 2.3 g/dL. Investigations confirmed cold agglutinin disease, validating the severe immune dysregulation predicted by the genotype. The patient responded to corticosteroid therapy and is currently awaiting hematopoietic stem cell transplantation (HSCT) from his HLA-compatible father. This report illustrates that early integration of WES in complex pediatric cases is essential to anticipate and manage severe complications, shifting the clinical focus from supportive care to curative interventions like HSCT. - Source: PubMed
Publication date: 2026/08/06
Hsairi MKammoun AFendri HGuirat MKammoun HMnif ZGargouri L - Serine/threonine kinase 4 (STK4) deficiency is one of the rare causes of combined immunodeficiency (CID). In this study, we report a novel mutation causing STK4 deficiency, which presents with chronic pyelonephritis, an uncommon presentation. - Source: PubMed
Publication date: 2026/08/14
Ashayeri HamidrezaEskandarzadeh ShabnamAlavi SaminSaberi MohammadReshadmanesh Azadeh - - Source: PubMed
Publication date: 2026/07/21
Govorov IgorAttarha SanazKovalevska LarysaAndersson EmilKashuba ElenaMints Miriam