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A Novel STK4 Mutation Presenting with Juvenile Idiopathic Arthritis.
MiR-135b was found to regulate MST1 (Stk4).
These results reveal that TRAF6 regulates YAP signaling by promoting the ubiquitination and degradation of MST1(STK4) in pancreatic cancer.
MST1 is a potential biomarker for early detection, prognosis and prediction of distant metastasis of colorectal cancer
confirmed the anti-proliferative, pro-apoptotic and pro-autophagy capabilities of TNRC6C-AS1 through STK4 methylation via the Hippo signalling pathway in thyroid carcinoma
the crucial role played by Smad2 in promoting Mst1(STK4)-mediated cell apoptosis and mitochondrial stress, is reported.
the comprehensive role of Mst1 (STK4) in colorectal cancer stress response involving apoptosis, mobilization, and growth via handling mitophagy by JNK/p53/Bnip3 pathways, is reported.
results define the Mst1 (STK4)/Drp1/mitochondrial fission/F-actin axis as a new signaling pathway that mediates LPS-related septic cardiomyopathy by inducing mitochondrial stress and cardiomyocyte death.
Because of divergent evolution of key interface residues, MST4 and MOB4 could disrupt assembly of the MST1-MOB1 complex through alternative pairing and thereby increased YAP activity. Collectively, these findings identify the MST4-MOB4 complex as a noncanonical regulator of the Hippo-YAP pathway with an oncogenic role in PC.
MST1 (Stk4) is involved in establishing endothelial tip cell polarity during sprouting angiogenesis.MST1 regulates FOXO1 localization at tip endothelial cells.
Study identified Mst1(Ste20-like kinase/STK4) as the primary pathogenesis for the development and progression of renal I/R injury via activation of fatal mitochondrial fission by modulating Drp1 phosphorylation, microtubule cytoskeleton dynamics, and the GSK3beta-p53 signalling pathway.
Results show that Mst1 is downregulated in non-small cell lung cancer (NSCLC) A549 cells, and overexpression of Mst1 promotes A549 cell apoptosis. Mst1 affects mitochondrial injury via the ROCK1/F-actin pathway highlighting the possibility that Mst1 dysregulation may be involved in the ability of NSCLC tumor cells to escape programmed cell death.
Diabetic stimuli lead to the activation of MST1, which impairs pancreatic beta-cell survival and function. [review]
hWW45 is required to enhance MST1-mediated apoptosis in vivo and thus is a critical player in an MST1-driven cell death signaling pathway.
MST1-FOXO1 signaling is an important link survival factor deprivation-induced neuronal cell death
hSav1 is a newly identified protein that interacts with Mst1 and augments Mst1-mediated apoptosis.
tolerance to increased levels of intracellular ROS provided by the Mst1-FoxOs signaling pathway is crucial for the maintenance of naive T cell homeostasis in the periphery
The identified Mst1 as a binding partner that interacts with PHLPPs both in vivo and in vitro. PHLPPs dephosphorylate Mst1 on the T387 inhibitory site, which activate Mst1 and its downstream effectors p38 and JNK to induce apoptosis.
H2AX is a substrate of MST1, which functions to induce apoptotic chromatin condensation and DNA fragmentation
novel regulatory mechanism involving the phosphorylation of Sirt1 by MST1 kinase which leads to p53 activation, with implications for our understanding of signaling mechanisms during DNA damage-induced apoptosis
MST1 (Stk4) plays a key regulatory role in neuronal cell death and cognition in high-fat diet (via JNK/Casp3 Signaling Pathway).
this study shows that Mst1 is required for long-lived humoral immunity
Stk3/4 (Mst1/2) are important regulators for glucose uptake during osteoblast differentiation.
Mst1 (Stk4) and Mst2 (Stk3) are therefore required for follicular B cells to acquire the ability to recirculate and also to migrate to the splenic red pulp in order to generate marginal zone B cells. In addition B-1 a B cell development is defective in the absence of Mst1.
Suramin modulated Mst1 (Stk4) expression.
Mst1 deficiency sends a pro-survival signal for the reperfused heart by reversing FUNDC1-related mitophagy and thus reducing cardiomyocyte mitochondrial apoptosis, which identifies Mst1 as a novel regulator for cardiac reperfusion injury via modulation of mitochondrial homeostasis.
our study reveals a role of Mst1-Mst2 in maintaining the Treg cell pool and functional fitness in vivo, by amplifying IL-2R-STAT5 signal strength and promoting Treg cell migratory ability and access to IL-2.
Data show that the kinases Mst1 and Mst2 (Mst1/2) sense ROS and maintain cellular redox balance by modulating the stability of antioxidant transcription factor Nrf2.
These results demonstrate that the pathogenesis of renal Ischaemia-Reperfusion Injury is closely associated with an increase in Mst1 expression and the inactive AMPK-YAP-OPA1 signalling pathway.
Study in experimental diabetes model utilizing endothelial-specific Mst1 transgenic mice exemplifies pleiotropic effects of Mst1-enriched exosomes released from cardiac microvascular endothelial cells on inhibiting autophagy, promoting apoptosis and suppressing the glucose metabolism in cardiomyocytes.
Results indicate the dendritic cell (DC) mammalian sterile 20-like kinase 1 (MST1)-p38MAPK signalling pathway in directing Th17 differentiation.
findings identify Mst1/2 as selective drivers of CD8alpha(+) dendritic cell function by integrating metabolic activity and cytokine signalling, and highlight that the interplay between immune signalling and metabolic reprogramming underlies the unique functions of dendritic cell subsets
NDR1 kinase, activated by the Rap1 signaling cascade through RAPL and Mst1/Mst2, associated with and recruited kindlin-3 to the immunological synapses, which was required for high-affinity LFA-1/ICAM-1 binding.[Kindlin-3]
the present study demonstrated that deletion of Mst1 attenuated neuronal loss and improved locomotor function in a mouse model of spinal cord injury, via preserving mitochondrial function, attenuating mitochondria-mediated apoptotic pathway, and suppressing inflammation, at least in part.
Mst1 deficiency promotes post-traumatic spinal motor neuron survival via enhancement of autophagy flux.
mammalian sterile 20-like kinase 1 (Mst1) knockout abolished the protective effects of Luteolin administration in a mouse model of myocardial infarction.
Studies indicate that Hippo (Hpo; MST1/2 in mammals) signaling pathway plays a central role in the cell fate-specification process.
Data (including data from studies in knockout/transgenic mice) suggest Mst1 has functional roles in cytotoxic T-lymphocytes and in inhibition of tumor progression/size of T-cell lymphoma; Mst1 may be involved in tumor immunity/immunologic surveillance.
the TLR-Mst1-Mst2-Rac signaling axis is critical for effective phagosome-mitochondrion function and bactericidal activity
The protein encoded by this gene is a cytoplasmic kinase that is structurally similar to the yeast Ste20p kinase, which acts upstream of the stress-induced mitogen-activated protein kinase cascade. The encoded protein can phosphorylate myelin basic protein and undergoes autophosphorylation. A caspase-cleaved fragment of the encoded protein has been shown to be capable of phosphorylating histone H2B. The particular phosphorylation catalyzed by this protein has been correlated with apoptosis, and it's possible that this protein induces the chromatin condensation observed in this process.
, STE20-like kinase MST1
, dJ211D12.2 (serine/threonine kinase 4 (MST1, KRS2))
, kinase responsive to stress 2
, mammalian STE20-like protein kinase 1
, mammalian sterile 20-like 1
, serine/threonine-protein kinase 4
, serine/threonine-protein kinase Krs-2
, Yeast Sps1/Ste20-related kinase 3
, sterile 20-like kinase 1