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Showing 1 to 4 of 4 for “"Molecular, Cellular, Developmental Biology and Genetics"”.

  1. Molecular and genetic characterization of spinocerebellar ataxia type 5 (SCA5)

    … 11 using an 11-generation American kindred, and was later refined to 11q13. Using a multifaceted mapping approach, which involved screening for expansion mutations, searching for haplotype conservation and sequencing, we discovered β-III spectrin (SPTBN2) mutations cause SCA5 in the American …

    umn Repository record for Molecular and genetic characterization of spinocerebellar ataxia type 5 (SCA5) (opens in a new tab)

  2. A biochemical and molecular analysis of functional differences between dystrophin and utrophin

    … for linking the actin cytoskeleton to the extracellular matrix via the dystrophin-glycoprotein complex. Mutations in dystrophin that abolish its expression lead to Duchenne muscular dystrophy (DMD). Patients with DMD become wheelchair bound in their early teens and succumb to fatal cardiac …

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  3. Activin signaling promotes the competence of the prothoracic gland during Drosophila metamorphosis

    … hormone ecdysone produced by the prothoracic gland. However, the molecular mechanisms that control production of the ecdysone titer are not completely understood. Here we show that blocking Activin signaling in Drosophila prothoracic gland causes developmental arrest prior to metamorphosis. This …

    umn Repository record for Activin signaling promotes the competence of the prothoracic gland during Drosophila metamorphosis (opens in a new tab)

  4. Oncogenic roles of RAS in acute myeloid leukemia cooperated with Mll-AF9.

    … including bone marrow-derived mast cells (BMMC) and CD34 positive hematopoietic progenitor cells (HPC) as well as myeloid and lymphoid lineages by live mouse imaging and relative light unit measurement before or after treating Vav-tTA ; TRE -luciferase co-transgenic mice with doxycycline (Dox). …

    umn Repository record for Oncogenic roles of RAS in acute myeloid leukemia cooperated with Mll-AF9. (opens in a new tab)