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show specific evidence for a cell-autonomous requirement for Msi family proteins in regulating stem cell differentiation, leading to the identification of an RNA-binding protein required for spermatogonial stem cell maintenance
we demonstrated the value of combined treatments with luteolin and olaparib (PARP inhibitor) or ionizing radiation (IR). Our results show that luteolin functions as an inhibitor of Msi1 and demonstrates its potential use in glioblastoma therapy.
This provides proof of concept for the development of Gn-lip as a molecular therapy for colon cancer with MSI1/MSI2 overexpression.
findings indicate that MSI1 plays a leading role in stress granule formation that grants cancer stem cell properties and chemoresistant stress granules in GBM, in response to stressful conditions via the PKR/eIF2alpha signalling cascade.
Enhanced expression of Musashi-1 was observed in adenomyosis foci in comparison with endometrial cells. The most intensive staining was found in nodular adenomyosis, especially in epithelial cells during the secretion phase. These data attest to the role of somatic stem cells in the development and progression of various forms of adenomyosis.
Msi1 acts as a stemness-associated gene in esophageal cancer cell lines and could serve as a prognostic marker in patients with ESCC.
MSI1 and MSI2 bind and regulate the mRNA stability and translation of proteins operating in essential oncogenic signaling pathways..This review provides a current overview of Musashi as a cancer driver and novel therapeutic target.
Musashi-1 has a role in regulating AKT-derived IL-6 autocrinal/paracrinal malignancy and chemoresistance in glioblastoma
MSI1 was a target of miR-181a-5p, a microRNA involved in the regulation of cancer development. The expression levels of MSI1 and miR-181a-5p were negatively correlated in NSCLC.
Musashi-1 interacts with the Zika genome and enables viral replication.
Msi1promoted epithelial-mesenchymal transformation of cervical neoplasms via activation of the Wnt signaling pathway and contributing to poor prognosis.
our results suggest a role for MSI1 in double-strand break repair and that its inhibition may enhance the effect of radiotherapy
Results show that Meis1 may have a positive feedback with Msi1 during the esophageal squamous cell carcinoma progression.
Musashi-1 expression was higher in Barrett esophagus and early esophageal adenocarcinoma compared to advanced adenocarcinoma.
miR-761 and MSI1 are inversely expressed in ovarian cancer tissues. In conclusion, we demonstrated that miR-761 repressed ovarian cancer proliferation and invasion by targeting MSI1
Concomitant loss of function of both MSI1 is sufficient to abrogate the growth of human colorectal cancer cells, and Msi gene deletion inhibits tumorigenesis in several mouse models of intestinal cancer.
Msi1 overexpression is associated with Esophageal Squamous Cell Carcinoma.
studies highlight Msi reporters as a unique tool to identify therapy resistance, and define Msi signalling as a central regulator of pancreatic cancer
Musashi-1 and ALDH1 expression are closely related to metastasis of ovarian adenocarcinoma.
Suggest high level of Musashi-1 protein expression is associated with poor survival in endometrioid adenocarcinoma patients.
Our results demonstrate that miR-137 acts as a tumor-suppressive miRNA in colorectal cancers and negatively regulates oncogenic Musashi-1
Msi1 has two RNA-binding domains.
leptin's direct stimulatory actions on gonadotrope GnRHR correlate with a direct inhibition of expression of the posttranscriptional regulator MSI1. There also is a direct MSI1 interaction with 3'-UTR of Gnrhr mRNA.
Msi proteins are dispensable for normal homeostasis and self-renewal of the active intestinal stem cell.
photoreceptors lack prototypical neuronal splicing factors and their splicing profile is driven to a significant degree by the Musashi 1 (MSI1) protein. A striking feature of the photoreceptor splicing program are exons that display a "switch-like" pattern of high inclusion levels in photoreceptors and near complete exclusion outside of the retina.
Given that deregulated fatty acid metabolism plays a key role in kidney fibrosis, these results demonstrate a novel connection between fatty acid and Msi1, an RNA-binding protein, in kidney fibrosis
A Mouse Model of Targeted Musashi1 Expression in Whole Intestinal Epithelium Suggests Regulatory Roles in Cell Cycle and Stemness.
the RNA-binding protein Musashi 1 competes with miR130a and -206 for interaction with tachykinin mRNA
MSI1 and MSI2 display distinct expression profiles during mammalian folliculogenesis and that MSI2 is required for pre-antral follicle development
Osteoarticular expression of Msi1 protein is increased in joints with CIA-induced lesion and absent in nonlesioned joints, suggesting that this protein is expressed when the lesion is produced in order to favor tissue repair.
Msi1 is critical for constructing functional blood-testis barrier &maintaining spermatogenesis. Msi1 regulates Sertoli cell fate following heat-induced injury, likely through induction of stress granule formation & activation of p-ERK1/2 signaling
Through expression studies and utilizing a transgenic Msi1 testis-specific overexpression model, we have identified 2 unique RNA-binding targets of MSI1 in spermatogonia, Msi2 and Erh, and have demonstrated a role for MSI1 in translational regulation.
Msi proteins contribute to an epithelial gene expression program in neural and mammary cell types.
MSI1 is specifically inhibited by 18-22 carbon omega-9 monounsaturated fatty acids; MSI1 regulates stearoyl-CoA desaturase
This study suggests that ciliogenic Rfx transcription factors regulate Msi1 expression in neural stem/progenitor cells.
Musashi1 binds to the Musashi binding element and that this element is required for polyadenylation in oocytes.
Msi1-dependent post-transcriptional enhancement of m-Numb is crucial in gastric epithelial regeneration.
RNA-binding protein Musashi1 modulates glioma cell growth through the post-transcriptional regulation of Notch and PI3 kinase/Akt signaling pathways.
data show that ectopic MSI1 expression may contribute to tumorigenesis in selected bladder cancers through multiple mechanisms and reveal a previously unrecognized function of Musashi1 in the regulation of SG formation
A regulatory element for Msi1 transcription in neural stem/progenitor cells is located in the sixth intron of the Msi1 gene.
Genome-wide analysis of CPEB1- and Msi1-associated mRNAs identified 491 common targets, thus revealing a new layer of cytoplasmic polyadenylation elements-mediated translational control.
specific association of Musashi with the noncanonical poly(A) polymerase germ line development defective-2 (GLD2)
Xenopus Musashi proteins regulate translation of the Musashi1 mRNA during oocyte maturation.
Ringo/cyclin-dependent kinase and mitogen-activated protein kinase signaling pathways regulate the activity of the cell fate determinant Musashi to promote cell cycle re-entry in Xenopus oocytes.
These findings indicate that Musashi function is necessary to establish the temporal order of maternal mRNA translation during Xenopus meiotic cell cycle progression.
Msi-1 expression is upregulated in the adult progenitor cells and plays important roles in their maintenance and/or active proliferation during amphibian gastrointestinal remodeling.
Visual deprivation for 2 days increased proliferation of musashi1-immunoreactive radial glial progenitors
This gene encodes a protein containing two conserved tandem RNA recognition motifs. Similar proteins in other species function as RNA-binding proteins and play central roles in posttranscriptional gene regulation. Expression of this gene has been correlated with the grade of the malignancy and proliferative activity in gliomas and melanomas. A pseudogene for this gene is located on chromosome 11q13.
, musashi homolog 1
, Musashi 1
, musashi 1
, RNA-binding protein Musashi homolog 1
, RNA-binding protein Musashi-1
, Musashi homolog 1(Drosophila)