Ask about this productRelated genes to: STK38L antibody
- Gene:
- STK38L NIH gene
- Name:
- serine/threonine kinase 38 like
- Previous symbol:
- -
- Synonyms:
- KIAA0965, NDR2
- Chromosome:
- 12p11.23
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-21
- Date modifiied:
- 2014-11-19
Related products to: STK38L antibody
Related articles to: STK38L antibody
- The Hippo pathway is a key regulator of development, regeneration, tissue homeostasis, and organ size, and its dysregulation promotes tumorigenesis. However, the precise mechanisms of its regulation in both normal physiology and cancer remain incompletely understood. Here, we identify STK38 and STK38L (also known as NDR1 and NDR2), previously proposed as redundant kinases of LATS, as negative regulators of the Hippo pathway. STK38/L inhibit LATS by competitively binding to MOB1 and disrupting the LATS-MOB1 complex, a process independent of their kinase activity. This inhibitory mechanism is evolutionarily conserved, as the ortholog Tricornered similarly impairs Warts-Mats complex formation, resulting in enlarged fly wing size. Pathologically, STK38L is highly expressed in ovarian cancer and required for ovarian tumor growth, and its amplification correlates with YAP activation and increased tumor sensitivity to TEAD inhibitors. Taken together, our study reveals a conserved role of STK38/L in Hippo pathway regulation, providing new insights into Hippo-dependent growth control and cancer development. - Source: PubMed
Publication date: 2026/07/01
An JeongminHuang ZhenKizhedathu AmruthaLan TianLin TzulingJoo HyejinThilakaratne Eshan MalindaLiu YuhanXu Yun YiYang BingLara-Gonzalez PabloWarrior RahulLuo RayWang Wenqi - Diabetic retinopathy (DR), a major complication of diabetes, is driven by chronic inflammation in which retinal microglial cells play a central role. The Hippo pathway kinases NDR1/2 regulate macrophage function, but their role in microglia and DR remain unknown. This study investigates the function of the NDR2 kinase in microglial cells under high-glucose (HG) conditions. Using CRISPR-Cas9, we partially knocked out the gene in BV-2 mouse microglial cells and analyzed metabolic activity, phagocytosis, migration, and cytokine release. We confirmed NDR2 expression in microglia and observed increased levels under HG, suggesting a role in hyperglycemia-induced stress. () downregulation impaired mitochondrial respiration and reduced metabolic flexibility, indicating defective stress adaptation. Functionally, microglia with a partial downregulation of displayed reduced phagocytic and migratory capacity-both dependent on cytoskeletal dynamics. Moreover, downregulation altered the secretory profile, elevating pro-inflammatory cytokines (IL-6, TNF, IL-17, IL-12p70) even under normal glucose levels. These findings identify NDR2 protein kinase as a key regulator of microglial metabolism and inflammatory behavior under diabetic conditions. By modulating immune and metabolic responses, NDR2 may contribute to the neuroinflammatory processes underlying DR. Targeting NDR2 function in microglia may offer novel therapeutic strategies to mitigate retinal inflammation and progression of DR. - Source: PubMed
Publication date: 2025/10/31
Fazendeiro BeatrizMachado IvoRolo AnabelaRodrigues Santos PauloAmbrósio António FranciscoSantos Paulo FLéger Hélène - : There is clear evidence for the higher prevalence of varicose veins (VVs) among women. In this regard, the research on sex differences affecting this condition is very important for sex-specific health care. We aimed to assess how male or female sex may contribute to the changes to gene expression profiles in the vein wall during varicose transformation. : Paired varicose vein (VV) and non-varicose vein (NV) segments were harvested from patients with VVs after venous surgery. Processed RNAs from those samples were subjected to gene expression analysis by reverse transcription quantitative polymerase chain reaction (RT-qPCR) followed by further data analysis. Multiple linear regression (MLR) analysis was performed to identify and characterize relationships among multiple factors (relative mRNA levels of a gene in NV or VV or their ratio, as dependent variables) and sex (independent variable, used individually or in combination with other patient's characteristics). For sex-specific gene regulation analysis, all potential binding sites for sex hormone receptors were identified in each gene's regulatory region sequence. : Using the independent method and a replicative patient sample set, we validated our previous data on 23 genes' differential expression in VVs and obtained insights on their sex-specific regulation. Sex (as an individual independent variable or in combination with other parameters-patient characteristics such as Age, BMI, CEAP class, Height, VVD manifestation and duration) was a moderate predictor (0.40 < R < 0.59; (R) < 0.05) for the expression in VVs (with its higher mRNA level in NVs and VVs of women compared to men); sex was a strong predictor (0.6 < R < 0.79; (R) < 0.05) for the expression in VVs (with its lower mRNA level in VVs of women compared to men); sex was a moderate predictor (0.40 < R < 0.59; (R) < 0.05) for the expression in NVs (with its lower mRNA level in NVs of women compared to men). : Confirmed differential expression of the studied genes in VVs indicates their plausible participation in vein wall remodeling. Sex-specific expression in veins for the subset of those genes suggests their hormonal regulation as well as other mechanisms involved in VV pathogenesis. This work enriches our understanding of sex features for the development of VVs and may provide the foundation for future investigations and beneficial treatment options. - Source: PubMed
Publication date: 2025/09/27
Smetanina Mariya AKorolenya Valeria ASevostyanova Ksenia SGavrilov Konstantin ASipin Fedor AShevela Andrey IFilipenko Maxim L - This study aimed to examine the changes in gene expression profiles of the bladder cancer cell line (HTB-9) after exposure with nanoliposomes (NLs) containing antisense miR-21, antisense miR-373, or a combination of both antisense miR-21 and antisense miR-373 oligonucleotides. - Source: PubMed
Publication date: 2025/05/12
Nikkhah OmidEinollahi BehzadAsadi MosaHeiat MohammadHushmandi Kiavash - The Rab11-Rabin8-Rab8 ciliogenesis complex regulates the expansion of cilia-derived light-sensing organelles, the rod outer segments, via post-Golgi rhodopsin transport carriers (RTCs). Rabin8 (also known as RAB3IP), an effector of Rab11 proteins and a nucleotide exchange factor (GEF) for Rab8 proteins, is phosphorylated at S272 by NDR2 kinase (also known as STK38L), the canine early retinal degeneration (erd) gene product linked to the human ciliopathy Leber congenital amaurosis (LCA). Here, we define the step at which NDR2 phosphorylates Rabin8 and regulates Rab11-to-Rab8 succession in Xenopus laevis transgenic rod photoreceptors expressing human GFP-Rabin8 and its mutants. GFP-Rabin8 accumulated with endogenous Rabin8 at the Golgi-apposed exit sites (GESs), also known as the trans-Golgi network (TGN). Rabin8 mutants deficient in Rab11 binding prevented membrane association of GFP-Rabin8. GFP-Rabin8 and NDR2 kinase both interacted with the RTC-associated R-SNARE VAMP7 at the trans-Golgi and the GESs. Here, GFP-Rabin8 and the phosphomimetic GFP-Rabin8-S272E integrated into RTCs, which were subsequently functionalized by Rabin8 Rab8 GEF activity. Non-phosphorylatable GFP-Rabin8-S272A caused significant GES enlargement and deformation, possibly leading to unconventional membrane advancement toward the cilium, bypassing RTCs. Rabin8 phosphorylation loss due to an NDR2 gene disruption thereby likely causes dysfunctional rhodopsin Golgi-to-cilia trafficking underlying retinal degeneration and early-onset blindness. - Source: PubMed
Publication date: 2025/01/23
Fresquez TheresaTam Beatrice MEshelman Shannon CMoritz Orson LRobichaux Michael ADeretic Dusanka