13,208 research outputs found

    Vascular endothelial growth factor restores delayed tumor progression in tumors depleted of macrophages

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    Genetic depletion of macrophages in Polyoma Middle T oncoprotein (PyMT)-induced mammary tumors in mice delayed the angiogenic switch and the progression to malignancy. To determine whether vascular endothelial growth factor A (VEGF-A) produced by tumor-associated macrophages regulated the onset of the angiogenic switch, a genetic approach was used to restore expression of VEGF-A into tumors at the benign stages. This stimulated formation of a high-density vessel network and in macrophage-depleted mice, was followed by accelerated tumor progression. The expression of VEGF-A led to a massive infiltration into the tumor of leukocytes that were mostly macrophages. This study suggests that macrophage-produced VEGF regulates malignant progression through stimulating tumor angiogenesis, leukocytic infiltration and tumor cell invasion

    LIN-41 does not function as an E3 ubiquitin ligase.

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    <p><b>A.</b> Sequence alignment of the mammalian TRIM71/LIN-41 RING domain with those from <i>Caenorhabditis</i> species and different known E3 ubiquitin ligases. Asterisks indicate the position of conserved cysteines (<i>C. elegans</i>: C114, C117, C130, C151, C154), which have been mutated to serines (S) to disrupt the domain (LIN-41<sup>RING</sup>). A highly conserved proline residue (P, highlighted in yellow), which is critical for canonical E3-E2 interactions, is absent in the nematode LIN-41 proteins. <b>B.</b> Fluorescent micrographs of live animals expressing wild-type (LIN-41<sup>WT</sup>) and mutated (LIN-41<sup>RING</sup>) GFP-tagged LIN-41 in the <i>lin-41(rrr3)</i> mutant background. The gonads are outlined with a dashed line. No differences in the distribution or in the levels of the two proteins have been observed (n>50). Scale bar: 20 µm.</p

    Welfare Implications of the Byrd Amendment

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    International Relations/Trade,
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