27 research outputs found

    CD146, a novel target of CD44-signaling, suppresses breast tumor cell invasion.

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    We have previously validated three novel CD44-downstream positively regulated transcriptional targets, including Cortactin, Survivin and TGF-β2, and further characterized the players underlying their separate signaling pathways. In the present study, we identified CD146 as a potential novel target, negatively regulated by CD44. While the exact function of CD146 in breast cancer (BC) is not completely understood, substantial evidence from our work and others support the hypothesis that CD146 is a suppressor of breast tumor progression. Therefore, using molecular and pharmacological approaches both in vitro and in breast tissues of human samples, the present study validated CD146 as a novel target of CD44-signaling suppressed during BC progression. Our results revealed that CD44 activation could cause a substantial decrease of CD146 expression with an equally notable converse effect upon CD44-siRNA inhibition. More interestingly, activation of CD44 decreased cellular CD146 and increased soluble CD146 through CD44-dependent activation of MMP. Here, we provide a possible mechanism by which CD146 suppresses BC progression as a target of CD44-downstream signaling, regulating neovascularization and cancer cell motility

    High angular resolution mm- and submm-observations of dense molecular gas in M82

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    Researchers observed CO(7-6), CO(3-2), HCN(3-2) and HCO+(3-2) line emission toward the starburst nucleus of M82 and have obtained an upper limit to H13CN(3-2). These are the first observations of the CO(7-6), HCN(3-2) and HCO+(3-2) lines in any extragalactic source. Researchers took the CO(7-6) spectrum in January 1988 at the Infrared Telescope Facility (IRTF) with the Max Planck Institute for Extraterrestrial Physics/Univ. of California, Berkeley 800 GHz Heterodyne Receiver. In March 1989 researchers used the Institute for Radio Astronomy in the Millimeter range (IRAM) 30 m telescope to observe the CO(3-2) line with the new MPE 350 GHz Superconductor Insulator Superconductor (SIS) receiver and the HCN(3-2) and HCO+(3-2) lines with the (IRAM) 230 GHz SIS receiver (beam 12" FWHM, Blundell et al. 1988). The observational parameters are summarized

    IKK/NF-κB regulates skeletal myogenesis via a signaling switch to inhibit differentiation and promote mitochondrial biogenesis

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    Nuclear factor κB (NF-κB) is involved in multiple skeletal muscle disorders, but how it functions in differentiation remains elusive given that both anti- and promyogenic activities have been described. In this study, we resolve this by showing that myogenesis is controlled by opposing NF-κB signaling pathways. We find that myogenesis is enhanced in MyoD-expressing fibroblasts deficient in classical pathway components RelA/p65, inhibitor of κB kinase β (IKKβ), or IKKγ. Similar increases occur in myoblasts lacking RelA/p65 or IKKβ, and muscles from RelA/p65 or IKKβ mutant mice also contain higher fiber numbers. Moreover, we show that during differentiation, classical NF-κB signaling decreases, whereas the induction of alternative members IKKα, RelB, and p52 occurs late in myogenesis. Myotube formation does not require alternative signaling, but it is important for myotube maintenance in response to metabolic stress. Furthermore, overexpression or knockdown of IKKα regulates mitochondrial content and function, suggesting that alternative signaling stimulates mitochondrial biogenesis. Together, these data reveal a unique IKK/NF-κB signaling switch that functions to both inhibit differentiation and promote myotube homeostasis

    Unusual shock-excited oh maser emission in a young Planetary Nebula

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    © 2016. The American Astronomical Society. All rights reserved. We report on OH maser emission toward G336.644-0.695 (IRAS 16333-4807), which is a H2O maser-emitting Planetary Nebula (PN). We have detected 1612, 1667, and 1720 MHz OH masers at two epochs using the Australia Telescope Compact Array, hereby confirming it as the seventh known case of an OH-maser-emitting PN. This is only the second known PN showing 1720 MHz OH masers after K 3-35 and the only evolved stellar object with 1720 MHz OH masers as the strongest transition. This PN is one of a group of very young PNe. The 1612 MHz and 1667 MHz masers are at a similar velocity to the 22 GHz H2O masers, whereas the 1720 MHz masers show a variable spectrum, with several components spread over a higher velocity range (up to 36 km s-1). We also detect Zeeman splitting in the 1720 MHz transition at two epochs (with field strengths of ~2 to ~10 mG), which suggests the OH emission at 1720 MHz is formed in a magnetized environment. These 1720 MHz OH masers may trace short-lived equatorial ejections during the formation of the PN

    Edited for the AAMC by:

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    This report was produced by the AAMC Advisory Committee on Sexual Orientation, Gender Identity, and Sex Development, which helps the academic medicine community advance the health care of individuals who are LGBT, gender nonconforming, or born with a difference of sex development. For more information, please contact: Tiffani St.Cloud, C.P.C

    CD146, a novel target of CD44-signaling, suppresses breast tumor cell invasion

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    We have previously validated three novel CD44-downstream positively regulated transcriptional targets, including Cortactin, Survivin and TGF-β2, and further characterized the players underlying their separate signaling pathways. In the present study, we identified CD146 as a potential novel target, negatively regulated by CD44. While the exact function of CD146 in breast cancer (BC) is not completely understood, substantial evidence from our work and others support the hypothesis that CD146 is a suppressor of breast tumor progression. Therefore, using molecular and pharmacological approaches both in vitro and in breast tissues of human samples, the present study validated CD146 as a novel target of CD44-signaling suppressed during BC progression. Our results revealed that CD44 activation could cause a substantial decrease of CD146 expression with an equally notable converse effect upon CD44-siRNA inhibition. More interestingly, activation of CD44 decreased cellular CD146 and increased soluble CD146 through CD44-dependent activation of MMP. Here, we provide a possible mechanism by which CD146 suppresses BC progression as a target of CD44-downstream signaling, regulating neovascularization and cancer cell motility.Other Information Published in: Cell Communication and Signaling License: In CopyrightSee article on publisher's website: http://dx.doi.org/10.1186/s12964-017-0200-3</p
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