Mammalian Ste20-like protein kinase 3 plays a role in hypoxia-induced apoptosis of trophoblast cell line 3A-sub-E

Wu, Hung-Yi; Lin, Chia Ying; Chen, Tai Chang; Pan, Shien Tung; Yuan, Chiun‐Jye

doi:10.1016/j.biocel.2011.01.015

Cited by 19 publications

(14 citation statements)

References 54 publications

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“…These GCKIII sub-family kinases have been implicated in regulating a number of cellular functions (Schinkmann and Blenis, 1997; Huang et al, 2002; Irwin et al, 2006; Lu et al, 2006; Wu et al, 2008; Lorber et al, 2009; Fidalgo et al, 2010; Wu et al, 2011) and interact with CCM3 [also known as programmed cell death 10 (PDCD10)] (Rual et al, 2005; Fidalgo et al, 2010; Zheng et al, 2010; Ceccarelli et al, 2011; Kean et al, 2011). Mutations in the CCM3 gene as well as in two other structurally unrelated genes, CCM1 and CCM2 , were found in the familial forms of Cerebral Cavernous Malformations (CCM) (Faurobert and Albiges-Rizo, 2010; Cavalcanti et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

A Network of Interactions Enables CCM3 and STK24 to Coordinate UNC13D-Driven Vesicle Exocytosis in Neutrophils

et al. 2013

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SUMMARY Neutrophil degranulation plays an important role in acute innate immune responses and is tightly regulated because the granule contents can cause tissue damage. However, this regulation remains poorly understood. Here we identify the complex of STK24 and CCM3 as being an important regulator of neutrophil degranulation. Lack of either STK24 or CCM3 increases the release of a specific granule pool without affecting other neutrophil functions. STK24 appears to suppress exocytosis by interacting and competing with UNC13D C2B domain for lipid binding, whereas CCM3 has dual roles in exocytosis regulation. While CCM3 stabilizes STK24, it counteracts STK24-mediated inhibition of exocytosis by recruiting STK24 away from the C2B domain through its Ca2+-sensitive interaction with UNC13D C2A domain. This STK24/CCM3-regulated exocytosis plays an important role in protection of kidneys from ischemia-reperfusion injury. Together, these findings reveal a previously unknown function of the STK24 and CCM3 complex in the regulation of ligand-stimulated exocytosis.

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Section: Introductionmentioning

confidence: 99%

A Network of Interactions Enables CCM3 and STK24 to Coordinate UNC13D-Driven Vesicle Exocytosis in Neutrophils

et al. 2013

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“…As summarized in Table 1, there are reports that GCKIIIs activate [possibly by acting as MAP4Ks (MAPK kinase kinase kinases)] or do not activate MAPKs, and it is difficult to come to any consistent conclusions. MAPKs have even been placed upstream of MST3 [41]. GCKIIIs are also associated with the stimulation of apoptosis (as described below), although these effects may be secondary to their influence on other fundamental processes, such as cell migration and proliferation.…”

Section: Functional Roles Of Gckiiismentioning

confidence: 99%

“…More recently, it appears to us that an emerging common denominator in GCKIII-regulated responses is the close association of GCKIIIs with different microtubular networks facilitated by a variety of protein-protein interactions. Through these interactions, GCKIIIs (often in conjunction with CCM3/PDCD10) participate in cell migration and proliferation and perversely in cell protection or apoptosis (see, for example, [10,27,29,30,33,41]).…”

Section: Functional Roles Of Gckiiismentioning

confidence: 99%

SOcK, MiSTs, MASK and STicKs: the GCKIII (germinal centre kinase III) kinases and their heterologous protein–protein interactions

Sugden

McGuffin

Clerk

2013

Biochemical Journal

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The GCKIII (germinal centre kinase III) subfamily of the mammalian Ste20 (sterile 20)-like group of serine/threonine protein kinases comprises SOK1 (Ste20-like/oxidant-stress-response kinase 1), MST3 (mammalian Ste20-like kinase 3) and MST4. Initially, GCKIIIs were considered in the contexts of the regulation of mitogen-activated protein kinase cascades and apoptosis. More recently, their participation in multiprotein heterocomplexes has become apparent. In the present review, we discuss the structure and phosphorylation of GCKIIIs and then focus on their interactions with other proteins. GCKIIIs possess a highly-conserved, structured catalytic domain at the N-terminus and a less-well conserved C-terminal regulatory domain. GCKIIIs are activated by tonic autophosphorylation of a T-loop threonine residue and their phosphorylation is regulated primarily through protein serine/threonine phosphatases [especially PP2A (protein phosphatase 2A)]. The GCKIII regulatory domains are highly disorganized, but can interact with more structured proteins, particularly the CCM3 (cerebral cavernous malformation 3)/PDCD10 (programmed cell death 10) protein. We explore the role(s) of GCKIIIs (and CCM3/PDCD10) in STRIPAK (striatin-interacting phosphatase and kinase) complexes and their association with the cis-Golgi protein GOLGA2 (golgin A2; GM130). Recently, an interaction of GCKIIIs with MO25 has been identified. This exhibits similarities to the STRADα (STE20-related kinase adaptor α)-MO25 interaction (as in the LKB1-STRADα-MO25 heterotrimer) and, at least for MST3, the interaction may be enhanced by cis-autophosphorylation of its regulatory domain. In these various heterocomplexes, GCKIIIs associate with the Golgi apparatus, the centrosome and the nucleus, as well as with focal adhesions and cell junctions, and are probably involved in cell migration, polarity and proliferation. Finally, we consider the association of GCKIIIs with a number of human diseases, particularly cerebral cavernous malformations.

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“…In human placentas following at-term births and caesarean deliveries without labour, Wu et al (4) identified that MST3 served a crucial role in apoptosis and detected significantly increased MST3 expression, trophoblast apoptosis, oxidative stress and hypoxia, and reported that these events were significantly correlated. In their study, trophoblast apoptosis was induced by hypoxia via nitric oxide synthase activation, which generated diverse components including O 2 -that upregulated MST3 via JNK activation (5). Other previous study has investigated apoptotic genes in the placenta as contributors to spontaneous preterm birth (sPTB).…”

Section: Introductionmentioning

confidence: 99%

“…In response to hypoxia and oxidative stress, the signalling pathways of hypoxia-induced apoptosis in human trophoblasts are considered to involve activation and/or upregulation of certain genes, including c-Jun N-terminal kinase (JNK), a key apoptosis regulatory gene (4,5). JNK serves as a mediator, bridging upstream hypoxia and oxidative stress events and the downstream mammalian STE20-like protein kinase 3 (MST3) gene (the human counterpart of the protein serine/threonine kinase Ste20 in yeast), with subsequent caspase 3 (CASP3) activation (6).…”

Section: Introductionmentioning

confidence: 99%

Induction of the apoptotic pathway by oxidative stress in spontaneous preterm birth: Single nucleotide polymorphisms, maternal lifestyle factors and health status

et al. 2018

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Abstract. The purpose of the present study was to search for associations between spontaneous preterm birth (sPTB), single nucleotide polymorphisms (SNPs) associated with the apoptotic pathway as triggered by oxidative stress, maternal lifestyle and health status. SNP genotyping [rs7560 for c-Jun N-terminal kinase (JNK), rs9517320 for mammalian STE20-like protein kinase 3 (MST3), rs1049216 for caspase 3 (CASP3)] in the placenta and maternal blood of 300 controls with at-term birth and 43 cases of sPTB was performed. No association was identified in genotype frequencies or combinations of foetal/maternal genotypes between single SNPs and sPTB. The risk of sPTB was significantly reduced by physical activity and significantly increased by current hypertensive diseases, premature rupture of membranes (PROM) or preterm PROM (P-PROM) and previous sPTB. The TT/GA genotype of JNK/CASP3 in maternal blood and maternal health status (current hypertensive diseases, current PROM/ P-PROM, previous sPTB) were independently associated with sPTB. The present findings suggested that, independently of other maternal factors, pregnant women carrying the TT/GA genotype of JNK/CASP3 were more susceptible to sPTB than women bearing the GT/GA (our reference) genotype; that the apoptotic pathway triggered by oxidative stress was involved; and that genetic and non-genetic factors contributed to sPTB. Knowledge of these aspects may aid to improve the management of pregnancies by indicating the lifestyle to be adopted on the basis of sPTB susceptibility.

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Mammalian Ste20-like protein kinase 3 plays a role in hypoxia-induced apoptosis of trophoblast cell line 3A-sub-E

Cited by 19 publications

References 54 publications

A Network of Interactions Enables CCM3 and STK24 to Coordinate UNC13D-Driven Vesicle Exocytosis in Neutrophils

A Network of Interactions Enables CCM3 and STK24 to Coordinate UNC13D-Driven Vesicle Exocytosis in Neutrophils

SOcK, MiSTs, MASK and STicKs: the GCKIII (germinal centre kinase III) kinases and their heterologous protein–protein interactions

Induction of the apoptotic pathway by oxidative stress in spontaneous preterm birth: Single nucleotide polymorphisms, maternal lifestyle factors and health status

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