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Human MSN Protein expressed in HEK-293 Cells - ABIN2726221
Miyaji, Shahrizaila, Umapathi, Chan, Hirata, Yuki: Are ERM (ezrin/radixin/moesin) proteins targets for autoantibodies in demyelinating neuropathies? in Human immunology 2015
These results indicate a critical role for Moesin in both neuronal morphogenesis and long-term memory formation.
The distribution of Moesin in the nucleus suggests a function in transcription and the depletion of mRNA export factors Nup98 or its interacting partner, Rae1, leads to the nuclear accumulation of Moesin, suggesting that the nuclear function of the protein is linked to mRNA export
Data show that Moesin upregulation influences extra-centrosome behavior and robust bipolar spindle formation.
Btsz and Moesin guide luminal membrane morphogenesis through organizing actin.
The conserved C-terminal coiled-coil domain of Slik, which is necessary and sufficient for apical localization of the kinase in epithelial cells, is not required for Moesin phosphorylation but is critical for the growth-promoting function of Slik.
Early endocytosis maintains normal steady-state levels of Crumbs, which recruits apical phosphorylated (active) Moesin, which in turn regulates seamless tube shape through modulation of cortical actin filaments.
Moesin interacts with an unusual RhoGAP, Conundrum (Conu), and recruits it to the cell cortex to negatively regulate RhoA activity.
Moesin stabilizes microtubules via a direct interaction at the cell cortex.
Wgn-Moe signaling cascade plays a key role in photoreceptor target field innervations through cell autonomous and non-cell autonomous mechanisms.
Drosophila melanogaster protein phosphatase type 1 beta (flapwing) co-regulates dephosphorylation and altered activity of both Merlin and Moesin.
This study revealed a novel mechanism for controlling salivary gland lumen size, namely through Rho1-dependent actin polymerization and distribution and downregulation of apical phosphorylated moesin.
the Pp1-87B phosphatase restricts high Moesin activity to early mitosis and down-regulates Moesin at the polar cortex, after anaphase onset.
Epithelial cell without moesin show reduced cortical actin cytoskeleton, lack of junctional markers, detach from and migrate out of the epithelium suggesting a role of moesin in the stabilization of the apical-junctional domain. (Review)
PtdIns(4,5)P(2) binding is essential for moesin recruitment to the membrane and for its subsequent phosphorylation.
Crumbs interacts with moesin and beta(Heavy)-spectrin in the apical membrane skeleton of Drosophila.
Dmoesin is required during oogenesis for anchoring microfilaments to the oocyte cortex. Alteration of the actin cytoskeleton resulting from Dmoesin mutations impairs the localization of maternal determinants, thus disrupting antero-posterior polarity.
rosslinks actin and cell membrane in Drosophila oocytes and is required for OSKAR anchoring.
Moesin functions antagonistically to the Rho pathway to maintain epithelial integrity
reductions in Moesin levels in the wing disc cause the formation of wing-tissue vesicles and large thickenings of the vein, corresponding to breakdowns of epithelial continuity in the wing base and modifications of Hedgehog signalling in the wing blade
our results demonstrate a role for moesin in regulating synaptic growth in the Drosophila neuromuscular junction.
suggest that Ve-cadherin and Moesin1 function to establish and maintain apical/basal polarity during multicellular lumen formation in the intersegmental vessels
results suggest a new role for moesin, acting in a signalling pathway facilitating the differentiation of extraembryonic endoderm
The Ano1-moesin interaction limits Ano1 lateral membrane mobility and contributes to microvilli scaffolding, therefore stabilizing larger membrane structures. Collectively, these results reveal a newly identified role for Ano1 in shaping the plasma membrane during oogenesis, with broad implications for the regulation of microvilli in epithelia.
These results suggested that strong moesin expression by malignant cells may help to determine patients with oral squamous cell carcinoma and poor prognosis.
Up-regulation of moesin expression in glioblastoma cells resulted in more aggressive orthotopic glioblastoma growth in nude mice.
In lip squamous carcinoma, moesin expression was strong at the invasive tumor front and weak/negative in differentiated cells. There was no association between moesin expression and the clinicopathological variables, but high moesin was associated with lower 5- and 10-year overall and disease-free survival rates. Moesin may participate in oral carcinogenesis.
This review focuses on the role of moesin in microvascular permeability and angiogenesis, and on the involvement of Src and ROS in endothelial barrier disruption.
CPI-17 drives Ras activity and tumorigenesis in melanomas in a two-fold way; inactivation of the tumor suppressor merlin and activation of the growth promoting ERM family.
The authors demonstrated that the expression of MSN in glioma specimens were negatively correlated with miR-200c expression, and MSN overexpression rescued the phenotype about cell proliferation and invasion induced by miR-200c.
The expression pattern and subcellular localization of ezrin and moesin correlate with clinicopathological variables such as patients' age, tumor grade and hormonal status.
Moesin and merlin regulate urokinase receptor-dependent endothelial cell migration, adhesion and angiogenesis
The results reveal a supportive role of ERMs in cortical activities during cytokinesis, and also provide insight into the selective mechanism that preferentially associates cytokinesis-relevant proteins with the division site.
These results indicate that loss of miR-200c, as a consequence of p53 mutation, can upregulate Moesin oncogene and thus promote carcinogenesis in breast cancer
the administration of 10(-6) M retinoic acid (10-20 min) induces the activation of the migration-related proteins Moesin, FAK, and Paxillin in T-47D breast cancer cells.
Up-regulation of moesin expression in glioblastoma cells correlated with increases in cell proliferation, invasion and migration, suggesting moesin's role in glioblastoma progression.
this study identifies X-linked primary immunodeficiency associated with hemizygous mutations in the moesin gene
These results of this study may pave the way for exploiting moesin as a novel target for intervention in muscular dystrophy.
The present study showed over-expression of ezrin and moesin in colorectal carcinoma
These results indicate that the Thr 558 phosphorylation in moesin mediates endothelial angiogenesis. Advanced glycation end products promoted human umbilical vein endothelial cell angiogenesis by inducing moesin phosphorylation via RhoA/ROCK pathway.
Phospho-Ezrin/Radixin/Moesin (ERM) inhibit cell adhesion, and therefore, dephosphorylation of ERM proteins is essential for cell adhesion.Phospho-ERM induce formation and/or maintenance of spherical cell shape.
Moesin was required in HMGB1-induced F-actin rearrangement, hyperpermeability, and inflammatory responses. HMGB1 increased Thr558 phosphorylation of moesin. Moesin was elevated in sepsis.
results indicate Moesin may regulate cell motility through its interactions with MT1-MMP and E-cadherin/p120-catenin adhesion complex and cytoplasmic expression of Moesin correlates with nodal metastasis and poor prognosis of OSCCs
Intracellular sphingosine kinase 2-derived sphingosine-1-phosphate mediates epidermal growth factor-induced ezrin-radixin-moesin phosphorylation and cancer cell invasion.
Inactivation of SHIP2 leads to increased microvilli formation and solute reabsorption by the renal proximal tubule and was associated with hyperactivated ezrin/radixin/moesin proteins and increased Rho-GTP.
Collectively, these results implicate both moesin and myosin IIA in the regulation of phagolysosome biogenesis and in host defense against infections.
these findings underscore the importance of moesin in IL-15-dependent CD8+ Treg cell homeostasis and the control of self-tolerance
Moesin is an important regulator of the surface abundance and stability of TbetaRII and is important in facilitating the efficient generation of iTregs.
The expression of moesin was upregulated in cardiomyocytes under inflammation, inducing protrusion formation in a phosphorylation-dependent fashion.
this study shows that low neutrophil rolling in inflamed venules was impaired in moesin-deficient mice
High blood moesin levels were also observed in cecal ligation and puncture (CLP)-induced sepsis in mice. Administration of blocking moesin antibodies attenuated CLP-induced septic death.
An increase in moesin expression may contribute to the increased expression of P-gp in blood brain barrier endothelial cells, leading to the development of morphine analgesic tolerance.
phosphorylation-regulated interaction between the cytoplasmic tail of cell polarity protein crumbs and the actin-binding protein moesin
both moesin-mediated inhibition and its localized deactivation by myosin phosphatase are essential for neutrophil polarization and effective neutrophil tracking of pathogens.
A novel role for moesin in regulating clathrin-dependent S1PR1 internalization through clathrin-coated vesicles formation.
Moesin may be a potential drug target for inhibiting corneal fibrosis, and the details of moesin-related signaling pathways would be critical for understanding corneal fibrosis.
Findings indicate a function of moesin in lymphocyte homeostasis in regulating lymphocyte egress from lymphoid organs.
A Pak1-PP2A-ERM signaling axis mediates F-actin rearrangement and degranulation in mast cells.
the extracellular matrix molecule VN and its neuronal receptor TLCN play a pivotal role in the phosphorylation of ezrin/radixin/moesin proteins and the formation of phagocytic cup-like structures on neuronal dendrites
Ezrin/radixin/moesin are required for the purinergic P2X7 receptor (P2X7R)-dependent processing of the amyloid precursor protein.
increased moesin expression promotes EMT by regulating adhesion and contractile elements for changes in actin filament organization.
biomarker for the assessment of genotoxic carcinogens in lymphoma
Moesin is involved in AGE-induced retinal vascular endothelial dysfunction and the phosphorylation of moesin is triggered via ROCK and p38 MAPK activation.
Moesin (for membrane-organizing extension spike protein) is a member of the ERM family which includes ezrin and radixin. ERM proteins appear to function as cross-linkers between plasma membranes and actin-based cytoskeletons. Moesin is localized to filopodia and other membranous protrusions that are important for cell-cell recognition and signaling and for cell movement.
, membrane-organizing extension spike protein