|
|
| (46 intermediate revisions by 2 users not shown) |
| Line 1: |
Line 1: |
| {{Kafatos/Christophides Lab-Small-Blue}}
| | http://www.vet.upenn.edu/people/faculty-clinician-search/MICHAELPOVELONES |
| {|cellspacing="5" cellpadding="10" style="background:#ffffff; width: 500px;"
| |
| |-valign="top"
| |
| |style="background:#ffffff"|
| |
| [[Image:Kafatos-action-pove.jpg|left|200px]]
| |
| |style="background:#ffffff"|
| |
| | |
| | |
| | |
| <div style="padding: 10px; color: #ffffff; background-color: #3674C2; width: 300px">
| |
| <font size="5">'''Michael Povelones'''</font size>
| |
| </div> <BR>
| |
| | |
| <div style="padding: 10px; color: #ffffff; background-color: #3674C2; width: 300px">
| |
| <font size="3" color="#ffffff">Division of Cell & Molecular Biology<br>
| |
| Imperial College<br>
| |
| South Kensington Campus<br>
| |
| SAF Building<br>
| |
| London, SW7 2AZ<br>
| |
| United Kingdom<br>
| |
| </font size></div>
| |
| |}
| |
| | |
| __NOTOC__
| |
| | |
| {|cellspacing="5" cellpadding="10" style="background:#3674C2; width: 750px;"
| |
| |-valign="top"
| |
| |style="background:#ffffff"|
| |
| ===Education===
| |
| <font size="3">
| |
| * BA in Chemistry, Columbia University, New York, NY, USA<br>
| |
| * PhD in Developmental Biology, Stanford University, Stanford, CA, USA<br>
| |
| * Biology of Parasitism 2005, MBL, Woods Hole, MA<br></font>
| |
| |}
| |
| | |
| | |
| {|cellspacing="5" cellpadding="10" style="background:#3674C2; width: 750px;"
| |
| |-valign="top"
| |
| |style="background:#ffffff"|
| |
| | |
| ===Current Research Interests===
| |
| <font size="3">I am a postdoctoral fellow in the [[kafatos:Kafatos/Christophides Lab|Kafatos/Christophides Lab]] at [http://www.imperial.ac.uk/ Imperial College], London. Science is cool.</font>
| |
| |}
| |
| | |
| | |
| {|cellspacing="5" cellpadding="10" style="background:#3674C2; width: 750px;"
| |
| |-valign="top"
| |
| |style="background:#ffffff"|
| |
| ===Previous Research===
| |
| <font size="3">I received my doctoral degree at Stanford University in the laboratory of Roel Nusse. The focus of my research was understanding how the ''frizzled (fz)'' receptor in ''Drosophila'' functions in planar cell polarization (PCP) and Wnt-mediated cell fate specification. ''fz'' controls two different signal transduction pathways for each of these distinct developmental outcomes. How does a single receptor function in two signaling pathways? This work revealed that even though cell fate signaling requires a Wnt ligand, ''fz'' is not activated by any of the 7 ''Drosophila'' Wnt genes for its PCP function. Instead, ''fz'' has an intrinsic ability to control components of the PCP pathway and that it associates with pathway specific Wnt co-receptor for cell fate signaling. In addition, a structure-function analysis of ''fz'' suggested that, in addition to the Wnt binding site located in the extracellular cysteine-rich domain, there is a second Wnt-binding site within the transmembrane portion of the receptor.</font>
| |
| [[Image:Kafatos-pove-fz.png|right|220px]]
| |
| <div style="padding: 10px; color: #222222; background-color: #DBEAFF; width: 500px">
| |
| <biblio>
| |
| #embo2005 pmid=16163385
| |
| #genetics2005 pmid=16085697
| |
| #naturecellbio2002 pmid=12415278
| |
| </biblio>
| |
| </div>
| |
| | |
| | |
| <font size="3">I worked in the laboratory of Richard Ambron as an undergraduate at Columbia University. The focus of this research was the identification of intrinsic nerve injury signals. In addition to growth factor and electrophysiological responses, neurons posses axonal proteins with a masked nuclear localization sequence (NLS) that serve as a sensor for injury. These injury signals are activated and rapidly retrogradely transported to the neuronal cell body and into the nucleus following nerve crush injury. In the nucleus they function to initiate the transcriptional program for repair. My research focused on the identification of an NF-κB-like transcription factor in Aplysia and its function in nerve injury. Nerve regeneration following injury requires transcriptional activation of repair genes. Members NF-κB family of transcription factors are well-suited to play a role in nerve injury since they contain and masked NLS and are localized to the cytoplasm until activated. This work identified by electrophoretic mobility shift assay an NF-κB-like activity in axoplasm. Contrary to what was expected, this activity was rapidly inactivated in injured neurons. We hypothesized that in these neurons, NF-κB functions as a signal of homeostasis and must be inactivated following injury since it regulates genes that are incompatible with repair. </font>
| |
| <div style="padding: 10px; color: #222222; background-color: #DBEAFF; width: 500px">
| |
| <biblio>
| |
| #neurobiology2001a pmid=11257614
| |
| #neurobiology2001b pmid=11153011
| |
| #neuroscience1997 pmid=9185529
| |
| #neuroscience1996 pmid=8922402
| |
| </biblio>
| |
| </div>
| |
| |}
| |
