Paige L Kneer

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Since the advent of mouse targeted mutations, gene traps, an escalating use of a variety of complex transgenic manipulations, and large-scale chemical mutagenesis projects yielding many mutants with cardiovascular defects, it has become increasingly evident that defects within the heart and vascular system are largely responsible for the observed in utero(More)
Hemizygous deletion of chromosome 22q11 (del22q11) causes thymic, parathyroid, craniofacial and life-threatening cardiovascular birth defects in 1 in 4,000 infants. The del22q11 syndrome is likely caused by haploinsufficiency of TBX1, but its variable expressivity indicates the involvement of additional modifiers. Here, we report that absence of the Vegf164(More)
Na(+)/Ca(2+) exchanger (Ncx-1) is highly expressed in cardiomyocytes, is thought to be required to maintain a low intracellular Ca(2+) concentration, and may play a role in excitation-contraction coupling. Significantly, targeted deletion of Ncx-1 results in Ncx1-null embryos that do not have a spontaneously beating heart and die in utero. Ultrastructural(More)
1. The Mechanism of the promotion by insulin of protein synthesis in muscle. •. L. MANCHESTER. Dept . of Biochemis t ry , Un ive r s i ty College, London. The fact t h a t one of the ma jo r act ions of insulin on muscle is to s t imula te passage of glucose across the m e m b r a n e makes i t unl ikely ~hat effects of the hormone are to be seen in(More)