Disease relevance of Msi1

• In contrast, Msi-1 expression in gastric glands showing intestinal metaplasia (IM) became weaker than that in the glands without IM [1].
• Early dysplastic crypts and adenomas were also strongly Musashi-1 positive [2].

High impact information on Msi1

• Total RNA was isolated from sorted fractions and used for quantitative real-time reverse-transcription polymerase chain reaction to evaluate the expression of cell lineage markers and the intestinal stem-cell marker, Musashi-1 [3].
• In mammals, two members of this family, Musashi1 (Msi1) and Musashi2 (Msi2), are strongly coexpressed in neural precursor cells, including CNS stem cells [4].
• Furthermore, adenovirus-induced Msi1 expression resulted in the down-regulation of endogenous m-Numb protein expression [5].
• In gliogenesis, the persistent expression of m-Msi-1 was observed in cells of the astrocyte lineage ranging from proliferative glial precursors in the subventricular zone (SVZ) to differentiated astrocytes in the parenchyma [6].
• Postnatally, m-Msi-1 was expressed in proliferative neuronal precursors in the external granule cell layer of the cerebellum and in the anterior corner of the subventricular zone of the lateral ventricles [6].
• It has been demonstrated that Msi1 is upregulated in various human cancers including colorectal. siRNA-mediated knockdown of Msi1 results in tumor xenograft growth arrest via induction of mitotic catastrophe and downregulation of Notch-1 [7].

Biological context of Msi1

• The evolutionarily conserved Musashi family of RNA-binding proteins is associated with maintenance and/or asymmetric cell division of neural progenitor cells, and a mammalian Musashi protein is expressed in various epithelial stem/progenitor cells, including gut, stomach, and mammary gland [8].
• Correlation between Musashi-1 and c-hairy-1 expression and cell proliferation activity in the developing intestine and stomach of both chicken and mouse [9].
• In postnatal development, persistent expression of the transgene was observed in astrocyte lineage cells as was Msi1 [10].
• During later stages of gestation, expression of the transgene was largely restricted to the ventricular zone (VZ) in the CNS, similar to the expression of Msi1 [10].
• In rat gonads, the RNA binding protein Msi1 is expressed in both proliferating and nonproliferating Sertoli and granulosa cells [11].

Anatomical context of Msi1

• We suppose that this wide expression of Msi1 in supporting cells indicates that those cells might have the potential to become hair cell progenitors if injured, but that some other mechanisms strictly inhibit this ability [12].
• Musashi1 (Msi1) is an RNA-binding protein expressed in neural stem/progenitor cells, astroglial progenitor cells and astrocytes in the vertebrate central nervous system [12].
• To observe this, we investigated Msi1 expression in young adult mouse cochlea by immunohistochemistry using monoclonal antibody against Msi1 [12].
• Msi1 immunostaining was found in a variety of supporting cells but not in outer hair cells in the organ of Corti [12].
• Msi1 immunoreactivity became lost in hair cells after E14 in vestibule and after E16 in cochlea, whereas it persisted in supporting cells until adulthood [13].

Associations of Msi1 with chemical compounds

• Regulation of tau RNA maturation by thyroid hormone is mediated by the neural RNA-binding protein musashi-1 [14].
• Immunohistochemical staining showed that the virus-susceptible cells were positive for GFAP, nestin, and Musashi-1, and that most of the infected cells were positive for the proliferative cell nuclear antigen and labeled with bromodeoxyuridine [15].
• The new Musashi Institute of Technology Reactor Thermal Neutron Therapy Facility and the increased domestic production of boron-10 isotope have enlarged the therapeutic capacity to two dozen patients a year [16].

Other interactions of Msi1

• Musashi-1 and Hes1 were not expressed in Paneth cells [17].
• These SP cells were 6-fold enriched for ERalpha-positive cells and expressed several fold higher levels of the ERalpha, p21(CIP1) and Msi1 genes than non-SP cells [18].
• In neurosphere cultures from transgenic embryos in the late phase of neurogenesis, the transgene was expressed in some cells of neurospheres expressing Msi1 and nestin [10].
• Immunohistochemical studies demonstrated that at all ages examined (from Fetal Day 14.5 until adulthood) Msi1 protein was expressed in Sertoli cells [11].
• COPs expressed the stem cell markers nestin, Notch1, Musashi-1, and ABCG2 and showed the side population cell phenotype [19].

Analytical, diagnostic and therapeutic context of Msi1

• Immunohistochemistry revealed that Msi1 was expressed in all otocyst cells at embryonic day (E) 10 and 12 [13].
• To investigate the involvement of Msi1 in the inner ear development, we studied the expression of Msi1 in mouse inner ears with RT-PCR and immunohistochemistry [13].
• Msi1 mRNA was expressed in rat testis from birth until adulthood; in situ hybridization revealed silver grains within the seminiferous epithelium [11].

References