-
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
-
Our work describes an MST4-ATG4B signaling axis that influences glioblastoma autophagy and malignancy
-
Low MST-4 expression is associated with Graves' disease.
-
these data identify the MST4 kinase as a novel candidate to mediate human pituitary tumorigenesis in a hypoxic environment and position it as a potential therapeutic target.
-
Our results suggest that MST4, STK25 and PDCD10 are upregulated in prostate cancer and may play roles in prostate tumorigenesis. MST4 may be a helpful marker for identifying prostate cancer.
-
Findings reveal a mechanism by which TRAF6 is regulated and highlight a role for MST4 in limiting inflammatory responses.
-
This study describes the key role of MST4 in facilitating the epithelial-mesenchymal transition process in hepatocellular carcinoma
-
Mutation of this residue was sufficient to switch the phosphorylation site preference for multiple kinases, including the serine-specific kinase PAK4 and the threonine-specific kinase MST4.
-
CCM3 forms a stable complex with MST4 in vivo to promote cell proliferation and migration synergistically in a manner dependent on MST4 kinase activity.
-
In this review, the germinal center kinase III subfamily of mammalian Ste20 (sterile 20)-like group of serine/threonine protein kinases comprises Ste20-like/oxidant-stress-response kinase 1, MST3 mammalian Ste20-like kinase 3 and MST4.
-
crystal of the CCM3-MST4 C-terminal domain complex belonged to space group P4(1)2(1)2 or P4(3)2(1)2, with unit-cell parameters a = 69.10, b = 69.10, c = 117.57 A
-
cloning of a germinal center iii kinase that induces apoptosis
-
MST4 expression in prostate carcinoma tumor samples & cell lines correlated with tumorigenicity & AR status. Overexpression induced anchorage-independent growth & tumorigenesis.It may have a role in the signal transduction in prostate cancer progression.
-
Results show that PDCD10 modulation of ERK signaling is mediated by MST4, and that PDCD10 may be a regulatory adaptor necessary for MST4 function, suggesting a link between cerebral cavernous malformation and the ERK-MAPK cascade via PDCD10/MST4.
-
These data define a brush border induction pathway downstream of the Lkb1/Strad/Mo25 polarization complex, yet separate from other polarity events.
