Only in Titles

Search results for: STK24

paperclip

#38328521   2024/01/24 To Up

Genetics of psycho-emotional well-being: genome-wide association study and polygenic risk score analysis.

Psycho-emotional well-being is essential for living a life of satisfaction and fulfillment. However, depression and anxiety have become the leading mental health issues worldwide, according to the World Health Organization. Both disorders have been linked to stress and other psychological factors. Their genetic basis remains understudied.
Anna Yurievna Yakovchik, Darya V Tolynyova, Daria A Kashtanova, Ekaterina R Sutulova, Mikhail V Ivanov, Alexandra A Mamchur, Veronika V Erema, Lorena R Matkava, Mikhail V Terekhov, Antonina M Rumyantseva, Olga I Blinova, Aleksandra I Akinshina, Sergey I Mitrofanov, Vladimir S Yudin, Valentin V Makarov, Anton А Keskinov, Sergey A Kraevoy, Sergey M Yudin

2148 related Products with: Genetics of psycho-emotional well-being: genome-wide association study and polygenic risk score analysis.

1 module1 module 6 ml Ready-to-use 1 mg1 module1 module200 1 module1,000 tests

Related Pathways

paperclip

#38229183   2024/01/16 To Up

Protein Kinase STK24 Promotes Tumor Immune Evasion via the AKT-PD-L1 Axis.

Immunotherapy targeting PD-L1 is still ineffective for a wide variety of tumors with high unpredictability. Deploying combined immunotherapy with alternative targeting is practical to overcome this therapeutic resistance. Here, the deficiency of serine-threonine kinase STK24 is observed in tumor cells causing substantial attenuation of tumor growth in murine syngeneic models, a process relying on cytotoxic CD8 T and NK cells. Mechanistically, STK24 in tumor cells associates with and directly phosphorylates AKT at Thr21, which promotes AKT activation and subsequent PD-L1 induction. Deletion or inhibition of STK24, by contrast, blocks IFN-γ-mediated PD-L1 expression. Various murine models indicate that in vivo silencing of STK24 can significantly enhance the efficacy of the anti-PD-1 blockade strategy. Elevated STK24 levels are observed in patient specimens in multiple tumor types and inversely correlated with intratumoral infiltration of cytotoxic CD8 T cells and with patient survival. The study collectively identifies STK24 as a critical modulator of antitumor immunity, which engages in AKT and PD-L1/PD-1 signaling and is a promising target for combined immunotherapy.
Ning Wang, Yu Jiang, Mengjie Li, Haofei Wang, Jie Pan, Yang Tang, Shaofang Xie, Yunyang Xu, Xu Li, Xuefei Zhou, Pinglong Xu, Wenlong Lin, Xiaojian Wang

1492 related Products with: Protein Kinase STK24 Promotes Tumor Immune Evasion via the AKT-PD-L1 Axis.

100ug Lyophilized200IU100 μg1mg100ug100 ul100ug Lyophilized10 50 KU100ul100ug

Related Pathways

paperclip

#38084599   2023/12/12 To Up

Macromolecular Complex Including MLL3, Carabin and Calcineurin Regulates Cardiac Remodeling.

Cardiac hypertrophy is an intermediate stage in the development of heart failure. The structural and functional processes occurring in cardiac hypertrophy include extensive gene reprogramming, which is dependent on epigenetic regulation and chromatin remodeling. However, the chromatin remodelers and their regulatory functions involved in the pathogenesis of cardiac hypertrophy are not well characterized.
Roberto Pane, Loubna Laib, Karina Formoso, Maximin Détrait, Yannis Sainte-Marie, Florence Bourgailh, Nolan Ruffenach, Hanamée Faugeras, Ilias Simon, Emeline Lhuillier, Frank Lezoualc'h, Caroline Conte

1234 related Products with: Macromolecular Complex Including MLL3, Carabin and Calcineurin Regulates Cardiac Remodeling.

10 2 200 1 mg100ul2.5 mg100ug Lyophilized

Related Pathways

paperclip

#37490000   // To Up

STE20-type kinases MST3 and MST4 promote the progression of hepatocellular carcinoma: Evidence from human cell culture and expression profiling of liver biopsies.

Hepatocellular carcinoma (HCC) is one of the most fatal and fastest growing malignancies. Recently, nonalcoholic steatohepatitis (NASH), characterized by liver steatosis, inflammation, cell injury (hepatocyte ballooning), and different stages of fibrosis, has emerged as a major catalyst for HCC. Because the STE20-type kinases, MST3 and MST4, have been described as critical molecular regulators of NASH pathophysiology, we here focused on determining the relevance of these proteins in human HCC. By analyzing public datasets and in-house cohorts, we found that hepatic MST3 and MST4 expression was positively correlated with the incidence and severity of HCC. We also found that the silencing of both MST3 and MST4, but also either of them individually, markedly suppressed the tumorigenesis of human HCC cells including attenuated proliferation, migration, invasion, and epithelial-mesenchymal transition. Mechanistic investigations revealed lower activation of STAT3 signaling in MST3/MST4-deficient hepatocytes and identified GOLGA2 and STRIPAK complex as the binding partners of both MST3 and MST4. These findings reveal that MST3 and MST4 play a critical role in promoting the progression of HCC and suggest that targeting these kinases may provide a novel strategy for the treatment of liver cancer.
Mara Caputo, Ying Xia, Sumit Kumar Anand, Emmelie Cansby, Emma Andersson, Hanns-Ulrich Marschall, Alfred Königsrainer, Andreas Peter, Margit Mahlapuu

1008 related Products with: STE20-type kinases MST3 and MST4 promote the progression of hepatocellular carcinoma: Evidence from human cell culture and expression profiling of liver biopsies.

1 kit(96 Wells) 100ul100 extractions96T96tests1 kit(96 Wells)96tests1.00 flask

Related Pathways

paperclip

#37202821   2023/05/18 To Up

Molecular mechanisms involved in regulating protein activity and biological function of MST3.

Mammalian sterile 20-like (Ste20-like) protein kinase 3 (MST3) or serine/threonine-protein kinase 24 (STK24) is a serine/threonine protein kinase that belongs to the mammalian STE20-like protein kinase family. MST3 is a pleiotropic protein that plays a critical role in regulating a variety of events, including apoptosis, immune response, metabolism, hypertension, tumor progression, and development of the central nervous system. The MST3-mediated regulation is intricately related to protein activity, post-translational modification, and subcellular location. Here, we review the recent progress on the regulatory mechanisms against MST3 and its-mediated control of disease progression.
Jing Qiu, Junzhi Xiong, Lu Jiang, Xinmin Wang, Kebin Zhang, Hua Yu

2492 related Products with: Molecular mechanisms involved in regulating protein activity and biological function of MST3.

2 Pieces/Box50 ug10 ug1 Set1 Set1 Set1 Set1 Set1 Set1 Set1 Set5mg

Related Pathways

paperclip

#37181807   2023/05/04 To Up

STK24 Promotes Progression of LUAD and Modulates the Immune Microenvironment.

Recent studies have shown that serine/threonine-protein kinase 24 (STK24) plays an important role in cancer development. However, the significance of STK24 in lung adenocarcinoma (LUAD) remains to be determined. This study is aimed at investigating the significance of STK24 in LUAD.
Yadong Li, Yanhu Liu, Kun Wang, Dong Xue, Yiqin Huang, Zhenguo Tan, Yijiang Chen

1508 related Products with: STK24 Promotes Progression of LUAD and Modulates the Immune Microenvironment.

1100 ug10 mg21000 tests100ug

Related Pathways

paperclip

#37155619   2023/05/08 To Up

Epithelial polarization in the 3D matrix requires MST3 signaling to regulate ZO-1 position.

Apical-basal cell polarity must be tightly controlled for epithelial cyst and tubule formation, and these are important functional units in various epithelial organs. Polarization is achieved through the coordination of several molecules that divide cells into an apical domain and a basolateral domain, which are separated from tight and adherens junctions. Cdc42 regulates cytoskeletal organization and the tight junction protein ZO-1 at the apical margin of epithelial cell junctions. MST kinases control organ size through the regulation of cell proliferation and cell polarity. For example, MST1 relays the Rap1 signal to induce cell polarity and adhesion of lymphocytes. Our previous study showed that MST3 was involved in E-cadherin regulation and migration in MCF7 cells. In vivo, MST3 knockout mice exhibited higher ENaC expression at the apical site of renal tubules, resulting in hypertension. However, it was not clear whether MST3 was involved in cell polarity. Here, control MDCK cells, HA-MST3 and HA-MST3 kinase-dead (HA-MST3-KD) overexpressing MDCK cells were cultured in collagen or Matrigel. We found that the cysts of HA-MST3 cells were fewer and smaller than those of control MDCK cells; ZO-1 was delayed to the apical site of cysts and in cell-cell contact in the Ca2+ switch assay. However, HA-MST3-KD cells exhibited multilumen cysts. Intensive F-actin stress fibers were observed in HA-MST3 cells with higher Cdc42 activity; in contrast, HA-MST3-KD cells had lower Cdc42 activity and weaker F-actin staining. In this study, we identified a new MST3 function in the establishment of cell polarity through Cdc42 regulation.
Chee-Hong Chan, Pei Lin, Tse-Yen Yang, Bo-Ying Bao, Jhen-Yang Jhong, Yui-Ping Weng, Te-Hsiu Lee, Hui-Fen Cheng, Te-Ling Lu

2744 related Products with: Epithelial polarization in the 3D matrix requires MST3 signaling to regulate ZO-1 position.

100ug100ug 100ul100ul1mg1010mg 10 MG

Related Pathways

paperclip

#36858329   2023/02/27 To Up

Comparative genomics studies on the stk gene family in vertebrates: From the bighead carp (Hypophthalmichthys nobilis) genome.

The mammalian sterile 20-like (MST) family belongs to the serine/threonine protein kinase (STK) superfamily and participates in a variety of biological processes, such as cell apoptosis, polarity, migration, immune regulation, inflammatory responses, and cancer. In the economically important bighead carp (Hypophthalmichthys nobilis), the STK gene family and immune-related biological functions may be helpful in increasing its economic yield. However, the comprehensive role of STKs in the bighead carp remains unclear. In this study, the five stk sequences from the bighead carp were divided into two classes: stk3/4 and stk24/25/26. Gene structure and motif prediction analyses confirmed that stk is conserved in the bighead carp. Compared to 26 other vertebrate species, teleosts (including bighead carp) possess more stk members because of teleost-specific whole-genome duplication. Synteny analysis revealed that stk3, stk24, stk25, and stk26 have been relatively conserved in bighead carp during evolution. Meanwhile, stk4 was lost in most Cyprinid species, including bighead carp, during evolution. RNA-seq data revealed that STK expression was associated with various pathogens, and the expression of these STKs (Hnstk3, Hnstk24a, Hnstk24b, Hnstk25, and Hnstk26) was different in seven tissues of bighead carp. In addition, we showed that STK expression levels were dramatically altered in the head kidney and that stk24 was involved in defense against Aeromonas hydrophila. This study provides a molecular basis for the analysis of stk function in bighead carp, and can be used as a reference for further phylogenomics.
Yang Mao, Defeng Li, Rongrong Chen, Caifeng Ma, Junzhi Xiong, Kebin Zhang

2979 related Products with: Comparative genomics studies on the stk gene family in vertebrates: From the bighead carp (Hypophthalmichthys nobilis) genome.

120 µl500 Units

Related Pathways

paperclip

#36720310   2023/01/28 To Up

Serine/threonine-protein kinase STK24 induces tumorigenesis by regulating the STAT3/VEGFA signaling pathway.

Lung cancer is the most common cause of cancer-related death. Although anti-angiogenesis therapy has been effective in the treatment of nonsmall cell lung cancer (NSCLC), drug-resistance is a common challenge. Therefore, there is a need to develop new therapeutic strategies for NSCLC. Serine/threonine-protein kinase 24 (STK24), also known as MST3, belongs to the germinal center kinase III subfamily, and the biological function of STK24 in NSCLC tumorigenesis and tumor angiogenesis is still unclear. In this study, we demonstrated that STK24 was overexpressed in lung cancer tissues compared with normal lung tissues, and lung cancer patients with higher STK24 expression levels had shorter overall survival time. In addition, our in vitro assays using A549 and H226 cell lines revealed that the STK24 expression level of cancer cells was positively correlated with cancer cells proliferation, migration, invasion, and tumor angiogenesis ability; in vivo assays also demonstrated that silencing of STK24 dramatically inhibited tumor progress and tumor angiogenesis. To investigate a mechanism, we revealed that STK24 positively regulated the signal transducer and activator of transcription 3 (STAT3)/vascular endothelial growth factor A (VEGFA) signaling pathway by inhibiting polyubiquitin-proteasomal-mediated degradation of STAT3. Furthermore, we performed in vivo assays in BALB/c nude mice and in vitro assays to show that STK24-regulated tumor angiogenesis depends on STAT3. These findings deepened our understanding of tumor angiogenesis, and the STK24/STAT3/VEGFA signaling pathway might be a novel therapeutic target for NSCLC treatment.
Senyan Lai, Dao Wang, Wei Sun, Xiaonian Cao

2705 related Products with: Serine/threonine-protein kinase STK24 induces tumorigenesis by regulating the STAT3/VEGFA signaling pathway.

100 μg96T0.1 mg 100ul100ug1 Set101mg2 Pieces/Box100ug

Related Pathways

paperclip

#36692953   2023/03/08 To Up

Release of STK24/25 suppression on MEKK3 signaling in endothelial cells confers cerebral cavernous malformation.

Loss-of-function mutations in cerebral cavernous malformation (CCM) genes and gain-of-function mutation in the MAP3K3 gene encoding MEKK3 cause CCM. Deficiency of CCM proteins leads to the activation of MEKK3-KLF2/4 signaling, but it is not clear how this occurs. Here, we demonstrate that deletion of the CCM3 interacting kinases STK24/25 in endothelial cells causes defects in vascular patterning during development as well as CCM lesion formation during postnatal life. While permanent deletion of STK24/25 in endothelial cells caused developmental defects of the vascular system, inducible postnatal deletion of STK24/25 impaired angiogenesis in the retina and brain. More importantly, deletion of STK24/25 in neonatal mice led to the development of severe CCM lesions. At the molecular level, a hybrid protein consisting of the STK kinase domain and the MEKK3 interacting domain of CCM2 rescued the vascular phenotype caused by the loss of ccm gene function in zebrafish. Our study suggests that CCM2/3 proteins act as adapters to allow recruitment of STK24/25 to limit the constitutive MEKK3 activity, thus contributing to vessel stability. Loss of STK24/25 causes MEKK3 activation, leading to CCM lesion formation.
Xi Yang, Shi-Ting Wu, Rui Gao, Rui Wang, Yixuan Wang, Zhenkun Dong, Lu Wang, Chunxiao Qi, Xiaohong Wang, M Lienhard Schmitz, Renjing Liu, Zhiming Han, Lu Wang, Xiangjian Zheng

1438 related Products with: Release of STK24/25 suppression on MEKK3 signaling in endothelial cells confers cerebral cavernous malformation.

1.00 flask1.00 flask1.00 flask1.00 flask1.00 flask25ml1mg1.00 flask25ml1.00 flask1.00 flask

Related Pathways