MSI1

Last update 08 May 2025

Basic Info

Synonyms

MSI1, musashi RNA binding protein 1, Musashi-1

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Introduction

RNA binding protein that regulates the expression of target mRNAs at the translation level. Regulates expression of the NOTCH1 antagonist NUMB. Binds RNA containing the sequence 5'-GUUAGUUAGUUAGUU-3' and other sequences containing the pattern 5'-[GA]U(1-3)AGU-3'. May play a role in the proliferation and maintenance of stem cells in the central nervous system (By similarity).

100 Clinical Results associated with MSI1

100 Translational Medicine associated with MSI1

0 Patents (Medical) associated with MSI1

726

Literatures (Medical) associated with MSI1

12 May 2025·Brain Injury

Cerebral ischemia-reperfusion induces the expression of phoenixin receptor (GPR173) and adult neurogenesis marker proteins in the rat striatum

Article

Author: Pukowiec, Marta ; Sharma, Veerta ; Bogus, Katarzyna ; Worthington, John J. ; Piwowarczyk-Nowak, Aneta ; Pałasz, Artur ; Filipczyk, Łukasz ; Skałba, Władysław ; Suszka-Świtek, Aleksandra ; Mordecka-Chamera, Kinga

OBJECTIVEBrain ischemia is considered an extremely potent stress factor at the cellular and molecular level which may lead to massive neuronal death. Alternatively, short brain ischemia and reperfusion (I/R) can actually stimulate neurogenesis, angiogenesis and peptidergic signaling. There is little known about the potential effect of I/R on brain expression of the novel neuropeptide; phoenixin (PNX) and its receptor GPR173.METHODSThe study was carried out on adult male Wistar rats divided into seven groups: control, sham operation and 5 ischemic experimental groups across the time course of reperfusion. We examined mRNA and protein expression of GPR173 and neurogenesis markers Musashi-1, doublecortin (DCX), and Sox-2 in the striatum.RESULTSGPR-173 positive cells were found only in the ischemic hemisphere, where Musashi-1, DCX and Sox-2-positive cells were also observed. Gene expression analysis also showed a significant increase of GPR-173 mRNA level in the I/R striatum in comparison with the control one. Results confirm previous findings suggesting that I/R stimulates adult neurogenesis in the striatum and affects peptidergic signaling in this structure.CONCLUSIONSA very fast occurence of GPR-173 expression revealed in the striatum may potentially be exclusively related to neuroprotective neurochemical changes that occur in this region after I/R.

01 May 2025·Molecular Biotechnology

Resveratrol Inhibits Colorectal Cancer Cell Tumor Property by Activating the miR-769-5p/MSI1 Pathway

Article

Author: Fan, Dingwen ; Zhang, Liangliang ; Liu, Hongchang ; Hao, Liangliang

Resveratrol exhibits inhibitory effects on the progression of various cancers including colorectal cancer (CRC), however, the underlying mechanism in regulating CRC development remains elusive. The present study aims to uncover the role and molecular mechanism of resveratrol in modulating CRC cell tumor properties. NCM460 cells, LoVo cells, SW480 cells, and BALB/c nude mice were utilized in this study. RNA levels of miR-769-5p and musashi RNA-binding protein 1 (MSI1) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Protein expression was assessed by western blotting or immunohistochemistry assay. Cell viability was analyzed by CCK-8 assay, while cell proliferation and apoptosis were evaluated by 5-Ethynyl-2'-deoxyuridine assay and flow cytometry analysis. Cell migration was investigated by transwell and wound-healing assays. The association between miR-769-5p and MSI1 was identified by a dual-luciferase reporter assay. Tumor formation was analyzed using a xenograft mouse model assay. Compared to control groups, miR-769-5p expression was downregulated, while MSI1 expression was upregulated in CRC tissues and cells. Resveratrol treatment led to increased miR-769-5p expression and decreased MSI1 expression in CRC cells. Resveratrol treatment or miR-769-5p upregulation inhibited CRC cell proliferation and migration, and induced apoptosis. These effects were enhanced after combined treatment with resveratrol and miR-769-5p mimics. MSI1 was identified as a target of miR-769-5p, and its overexpression attenuated the effects of miR-769-5p mimics on cell proliferation, migration, and apoptosis. Moreover, miR-769-5p overexpression enhanced the inhibitory effects of resveratrol on tumor growth in vivo. Resveratrol inhibited colorectal cancer cell tumor properties by activating the miR-769-5p/MSI1 pathway.

01 Apr 2025·Progress in Neurobiology

Pathogenic oligomeric Tau alters neuronal RNA processes through the formation of nuclear heteromeric amyloids with RNA-binding protein Musashi1

Article

Author: Penalva, Luiz O ; Lugano, Doreen ; Fung, Leiana ; Hao, Haiping ; Samples, Madison ; Aday, Abbigael E ; Zhao, Yingxin ; Montalbano, Mauro ; Park, Suhyeorn J ; Bhatt, Nemil ; Cascio, Filippa Lo ; Kayed, Rakez ; Puangmalai, Nicha ; Marcatti, Michela ; Jerez, Cynthia

Alzheimer's disease (AD) is marked by cytoplasmic proteinopathies, primarily involving misfolded Tau protein. Pathogenic Tau species, such as soluble oligomers and fibrils, disrupt RNA metabolism, though the mechanisms are unclear. Recent research indicates that RNA has a crucial role in Tau aggregation. Our study builds on this by noting significant co-deposition of RNA-Binding Proteins (RBPs) with Tau in AD and Frontotemporal dementia (FTLD) brains. Using molecular and cellular techniques, we investigate the interaction between RNA dynamics and Tau aggregation, focusing on the localization and aggregation of Tau and RBPs, particularly Musashi (MSI), within neuronal nuclei. Through cyto-fluorometric, biochemical, and cellular assays, we reveal the importance of Tau/RBP interplay in primary cortical neurons expressing wild-type and mutant Tau. Pathogenic Tau oligomers alter MSI protein localization and function, causing cytoplasmic and nuclear aggregation. Mass spectrometry of the MSI1 nuclear interactome in Tau models shows disrupted RNA metabolism pathways, including ribosomal biogenesis, RNA splicing, and protein folding. Moreover, RNA immunoprecipitation assay revealed a remarkable impact of mutant P301L Tau on MSI1 ability to bind RNA targets. These findings highlight potential targets for early neurodegenerative therapeutic interventions.

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MSI1

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