139 research outputs found

    Leioscyta humeralis Goding

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    <i>Leioscyta humeralis</i> Goding <p> <i>Leioscyta humeralis</i> Goding 1930a: 91; Metcalf and Wade, 1965a: 1317; McKamey, 1998a: 207. Original repository: MPSP.</p> <p> <b>Holotype male</b> from BRAZIL: <i>São Paulo</i>: São Paulo: " SÃO PAULO \ <i>Ipiranga</i> ", "[red label] Cotype", " <i>Leioscyta</i> \ <i>humeralis</i> \ <i>Goding</i> ", "Coleção \ PINTO DA \ FONSECA". Double-mounted on minuten, mesothoracic legs lacking tarsomeres; pronotum broken, lacking distal tip of posterior process.</p> <p> <b>Remarks.</b> Goding (1930) also designated three paratypes (one male and two females): one originally deposited at MPSP and two deposited in his personal collection. However, the author did not specify the sex of paratypes in each repository. One paratype (gender not specified) was not located in the collection.</p>Published as part of <i>Evangelista, Olivia, Santos, Guilherme Ide Marques Dos & Lamas, Carlos Einicker, 2014, An annotated catalogue of the Membracidae types in the Museu de Zoologia da Universidade de São Paulo, Brazil (Hemiptera: Auchenorrhyncha: Cicadomorpha), pp. 1-30 in Zootaxa 3895 (1)</i> on page 19, DOI: 10.11646/zootaxa.3895.1.1, <a href="http://zenodo.org/record/287608">http://zenodo.org/record/287608</a&gt

    Fidicinoides distanti (Goding)

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    <p> <i>Fidicinoides distanti</i> (Goding)</p> <p> – the FSCA has specimens from Rondonia 62 km S Ariquemes, linea C- 20, 7 km E B-65, 165m, Fazenda Rancho Grande, 10 o 32’S 62 o 48’W, 14-22-III- 1990; and Rondonia, 60 km S Ariquemes, 17-24-III-1989.</p> <p> The author received a specimen from C. Covell collected in Rondonia, Fazenda Rancho Grande, vicinityof Cacaulandia, 15-III-1991. The species has recently been transferred to <i>Fidicinoides</i> Boulard and Martinelli (Sanborn 2007a)</p> <p>and was reported previously only from Ecuador (Goding 1925) and Venezuela (Sanborn 2007a).</p>Published as part of <i>Sanborn, Allen F., 2008, New Records of Brazilian Cicadas Including the Description of a New Species (Hemiptera: Cicadoidea, Cicadidae), pp. 685-690 in Neotropical Entomology 37 (6)</i> on page 689, DOI: 10.1590/s1519-566x2008000600010, <a href="http://zenodo.org/record/3557762">http://zenodo.org/record/3557762</a&gt

    Tbx3 represses E-cadherin expression and enhances melanoma invasiveness.

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    The T-box transcription factors Tbx2 and Tbx3 are overexpressed in many cancers and in melanoma promote proliferation by actively suppressing senescence. Whether they also contribute to tumor progression via other mechanisms is not known. Here, we identify a novel role for these factors, providing evidence that Tbx3, and potentially Tbx2, directly repress the expression of E-cadherin, a keratinocyte-melanoma adhesion molecule whose loss is required for the acquisition of an invasive phenotype. Overexpression of Tbx2 and Tbx3 in melanoma cells down-regulates endogenous E-cadherin expression, whereas depletion of Tbx3, but not Tbx2, increases E-cadherin mRNA and protein levels and decreases melanoma invasiveness in vitro. Consistent with these observations, in melanoma tissue, Tbx3 and E-cadherin expression are inversely correlated. Depletion of Tbx3 also leads to substantial up-regulation of Tbx2. The results suggest that Tbx2 and Tbx3 may play a dual role during the radial to vertical growth phase transition by both inhibiting senescence via repression of p21(CIP1) expression, and enhancing melanoma invasiveness by decreasing E-cadherin levels

    Melanosome-autonomous regulation of size and number: the OA1 receptor sustains PMEL expression.

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    Little is known as to how cells ensure that organelle size and number are coordinated to correctly couple organelle biogenesis to the demands of proliferation or differentiation. OA1 is a melanosome-associated G-protein-coupled receptor involved in melanosome biogenesis during melanocyte differentiation. Cells lacking OA1 contain fewer, but larger, mature melanosomes. Here, we show that OA1 loss of function reduces both the basal expression and the α-melanocyte-stimulating hormone/cAMP-dependent induction of the microphthalmia-associated transcription factor (MITF), the master regulator of melanocyte differentiation. In turn, this leads to a significant reduction in expression of PMEL, a major melanosomal structural protein, but does not affect tyrosinase and melanin levels. In line with its pivotal role in sensing melanosome maturation, OA1 expression rescues melanosome biogenesis, activates MITF expression and thereby coordinates melanosome size and number, providing a quality control mechanism for the organelle in which resides. Thus, resident sensor receptors can activate a transcriptional cascade to specifically promote organelle biogenesis

    The retinoblastoma protein modulates Tbx2 functional specificity

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    Tbx2 is a member of a large family of transcription factors defined by homology to the T-box DNA-binding domain. Tbx2 plays a key role in embryonic development, and in cancer through its capacity to suppress senescence and promote invasiveness. Despite its importance, little is known of how Tbx2 is regulated or how it achieves target gene specificity. Here we show that Tbx2 specifically associates with active hypophosphorylated retinoblastoma protein (Rb1), a known regulator of many transcription factors involved in cell cycle progression and cellular differentiation, but not with the Rb1-related proteins p107 or p130. The interaction with Rb1 maps to a domain immediately carboxy-terminal to the T-box and enhances Tbx2 DNA binding and transcriptional repression. Microarray analysis of melanoma cells expressing inducible dominant-negative Tbx2, comprising the T-box and either an intact or mutated Rb1 interaction domain, shows that Tbx2 regulates the expression of many genes involved in cell cycle control and that a mutation which disrupts the Rb1-Tbx2 interaction also affects Tbx2 target gene selectivity. Taken together, the data show that Rb1 is an important determinant of Tbx2 functional specificity

    Transcription and cancer.

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    The normal growth, development and function of an organism requires precise and co-ordinated control of gene expression. A major part of this control is exerted by regulating messenger RNA (mRNA) production and involves complex interactions between an array of transcriptionally active proteins and specific regulatory DNA sequences. The combination of such proteins and DNA sequences is specific for given gene or group of genes in a particular cell type and the proteins regulating the same gene may vary between cell types. In addition the expression or activity of these regulatory proteins may be modified depending on the state of differentiation of a cell or in response to an external stimulus. Thus, the differentiation of embryonic cells into diverse tissues is achieved and the mature structure and function of the organism is maintained. This review focusses on the role of perturbations of these transcriptional controls in neoplasia. Deregulation of transcription may result in the failure to express genes responsible for cellular differentiation, or alternatively, in the transcription of genes involved in cell division, through the inappropriate expression or activation of positively acting transcription factors and nuclear oncogenes. Whether the biochemical abnormalities that lead to the disordered growth and differentiation of a malignant tumour affect cell surface receptors, membrane or cytoplasmic signalling proteins or nuclear transcription factors, the end result is the inappropriate expression of some genes and failure to express others. Current research is starting to elucidate which of the elements of this complicated system are important in neoplasia
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