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  • Key basic helix-loop-helix transcription factor genes Hes1 and Ngn2 are regulated by Pax3 during mouse embryonic development. 18308300

    Pax3 is expressed early during embryonic development in spatially restricted domains including limb muscle, neural crest, and neural tube. Pax3 functions at the nodal point in melanocyte stem cell differentiation, cardiogenesis and neurogenesis. Additionally Pax3 has been implicated in migration and differentiation of precursor cell populations. Currently there are questions about how Pax3 regulates these diverse functions. In this study we found that in the absence of functional Pax3, as in Splotch embryos, the neural crest cells undergo premature neurogenesis, as evidenced by increased Brn3a positive staining in neural tube explants, in comparison with wild-type. Premature neurogenesis in the absence of functional Pax3 may be due to a change in the regulation of basic helix-loop-helix transcription factors implicated in proliferation and differentiation. Using promoter-luciferase activity measurements in transient co-transfection experiments and electro-mobility shift assays, we show that Pax3 regulates Hairy and enhancer of split homolog-1 (Hes1) and Neurogenin2 (Ngn2) by directly binding to their promoters. Chromatin immunoprecipitation assays confirmed that Pax3 bound to cis-regulatory elements within Hes1 and Ngn2 promoters. These observations suggest that Pax3 regulates Hes1 and Ngn2 and imply that it may couple migration with neural stem cell maintenance and neurogenesis.
    Document Type:
    Reference
    Product Catalog Number:
    AB5945
    Product Catalog Name:
    Anti-Brn-3a Antibody

  • Basic fibroblast growth factor supports expansion of mouse compact bone-derived mesenchymal stem cells (MSCs) and regeneration of bone from MSC in vivo. 22203245

    Some progress has been made in development of methods to regenerate bone from cultured cells, however no method is put to practical use. Here, we developed methods to isolate, purify, and expand mesenchymal stem cells (MSCs) from mouse compact bone that may be used to regenerate bone in vivo. These cells were maintained in long-term culture and were capable of differentiating along multiple lineages, including chondrocyte, osteocyte, and adipocyte trajectories. We used standard cell isolation and culture methods to establish cell cultures from mouse compact bone and bone marrow. Cultures were grown in four distinct media to determine the optimal composition of culture medium for bone-derived MSCs. Putative MSCs were subjected to flow cytometry, alkaline phosphatase assays, immunohistochemical staining, and several differentiation assays to assess cell identity, protein expression, and developmental potential. Finally, we used an in vivo bone formation assay to determine whether putative MSCs were capable of regenerating bone. We found that compact bone of mice was a better source of MCSs than the bone marrow, that growth in plastic flasks served to purify MSCs from hematopoietic cells, and that MSCs grown in basic fibroblast growth factor (bFGF)-conditioned medium were, based on multiple criteria, superior to those grown in leukemia inhibitory factor-conditioned medium. Moreover, we found that the MSCs isolated from compact bone and grown in bFGF-conditioned medium were capable of supporting bone formation in vivo. The methods and results described here have implications for understanding MSC biology and for clinical purpose.
    Document Type:
    Reference
    Product Catalog Number:
    MAB8887
    Product Catalog Name:
    Anti-Collagen Type II Antibody, clone 6B3

  • Basic protein dissociating from myelin membranes at physiological ionic strength and pH is cleaved into three major fragments. 2433395

    Experiments were performed with isolated human myelin membrane preparations to analyse factors that may modulate association of myelin basic protein (MBP) with the membranes and could contribute to demyelinating processes. Transfer of membranes (5 mg protein ml-1) at 37 degrees C and pH 7.4 from a hypotonic medium, in which they were relatively stable, to one of physiological ionic strength produced three major effects: (1) initial dissociation of MBP from the membranes by a nonenzymatic process that was doubled in the presence of millimolar Ca2+/Mg2+; (2) within 10 min, the appearance in the medium of three major MBP fragments (14.4, 10.3, and 8.4 kilodaltons); and (3) progressive acidification of dissociated MBP and its fragments, probably due to deamidation. Between 1 and 6 h a steady state was apparent in which protein equivalent to 15% of the MBP originally bound to the membranes was found in the medium. The three major MBP fragments formed two-thirds of this solubilised material and appeared metabolically stable for 24 h. The kinetics of peptide formation suggested that dissociated, rather than membrane-bound, MBP was cleaved by myelin-associated neutral proteases. Two-dimensional electrophoresis and immunoblotting using two monoclonal antibodies indicated that proteolysis occurred in the vicinity of residues 35 and 75. Evidence was also obtained for removal of C-terminal arginines and relatively rapid deamidation in the C-terminal half of MBP. These modifications of MBP might also occur if extracellular fluid gained access to the compacted cytoplasmic space of the myelin sheath.
    Document Type:
    Reference
    Product Catalog Number:
    MAB386
    Product Catalog Name:
    Anti-Myelin Basic Protein Antibody, a.a. 82-87

  • Myelin basic protein induces neuron-specific toxicity by directly damaging the neuronal plasma membrane. 25255088

    The central nervous system (CNS) insults may cause massive demyelination and lead to the release of myelin-associated proteins including its major component myelin basic protein (MBP). MBP is reported to induce glial activation but its effect on neurons is still little known. Here we found that MBP specifically bound to the extracellular surface of the neuronal plasma membrane and induced neurotoxicity in vitro. This effect of MBP on neurons was basicity-dependent because the binding was blocked by acidic lipids and competed by other basic proteins. Further studies revealed that MBP induced damage to neuronal membrane integrity and function by depolarizing the resting membrane potential, increasing the permeability to cations and other molecules, and decreasing the membrane fluidity. At last, artificial liposome vesicle assay showed that MBP directly disturbed acidic lipid bilayer and resulted in increased membrane permeability. These results revealed that MBP induces neurotoxicity through its direct interaction with acidic components on the extracellular surface of neuronal membrane, which may suggest a possible contribution of MBP to the pathogenesis in the CNS disorders with myelin damage.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • Acidic and basic fibroblast growth factor messenger RNA and protein show increased expression in adult compared to developing normal and dystrophic rat retina. 9356923

    To further elucidate the possible roles of fibroblast growth factors (FGFs) in retinal pathophysiology, messenger RNA levels of acidic and basic FGF (aFGF and bFGF, respectively) were measured throughout embryonic and postnatal development until adulthood in normal and dystrophic (Royal College of Surgeons, RCS) rat retinas using sensitive reverse transcription-coupled polymerase chain reaction (PCR) techniques. In normal rats, both aFGF and bFGF transcript levels remained steadily low throughout embryogenesis and up until 7 d of postnatal age. By 13 d bFGF mRNA had increased 30-fold, and by adulthood (4 mo) levels were 150 times greater than in newborn retina. Dystrophic RCS retinas followed the same basic pattern, except that bFGF expression levels were increased relative to normal rats: By 4 d postnatal RCS retinas contained three times more bFGF mRNA than normal, by 7 d they contained six times more, and by 10 d they contained eight times more. In contrast, aFGF mRNA levels rose only threefold between embryonic and adult stages, and did not show any differences between normal and RCS rats. In parallel, staining of lightly fixed frozen sections of young ( 20 d) normal rat retina with antibodies to bFGF revealed only faint labeling of neural cells, whereas adult retinal sections were labeled strongly, especially within the photoreceptor layer. Twenty-day RCS rat retina showed detectable bFGF-like immunoreactivity. Hence, these data indicate that major aFGF and bFGF expression occurs only late in retinal maturation, suggesting these factors act principally as survival factors, especially for photoreceptors. In addition, the increased expression in a degenerative mutant strain may indicate the early onset of general cellular stress.
    Document Type:
    Reference
    Product Catalog Number:
    05-118
    Product Catalog Name:
    Anti-FGF-2/basic FGF Antibody, clone bFM-2