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UID:1026@biology.technion.ac.il

DTSTART;TZID=Asia/Jerusalem:20211215T133000

DTEND;TZID=Asia/Jerusalem:20211215T140000

DTSTAMP:20211212T125810Z

URL:https://biology.technion.ac.il/en/seminars/msc-graduate-seminar-kapil-
 jain/

SUMMARY:MSC Graduate Seminar-Kapil Jain [No Categories]
DESCRIPTION:Location:   \n Affiliation: \n Host:\n Regulation of mitochondr
 ial trafficking by Myosin XIX during cell migration.\n\n Myosin XIX (Myo19
 ) is an actin-based molecular motor that is anchored to the outer mitochon
 dria membrane (OMM) via its unique membrane binding motif. Myo19 is a stro
 ng effector of filopodia formation under cellular stress conditions mediat
 ed by glucose starvation\, ROS and EGF. Filopodia are actin protrusions im
 portant for many cellular dynamic processes such as cell migration\, angio
 genesis\, wound healing\, limb regeneration and sensing extracellular envi
 ronment\, among others. In mammals\, Myo19’s ability to induce filopodia
  is strongly coupled to mitochondrial transport on the actin filaments whi
 ch is achieved by the enzymatic adaptation of its active motor as an ensem
 ble of molecules bound to mitochondria. However\, the cellular processes w
 hich are essentially required for triggering Myo19 based mitochondrial mot
 ility to filopodia are not known. In addition\, the role of these mitochon
 dria rich filopodia actin protrusions are yet to be coupled to their cellu
 lar functions. Cell migration being a fundamental process in both physiolo
 gy and pathophysiology requires actin cytoskeleton remodeling\, and hence 
 we hypothesize that Myo19 will play a role during cell migration. Interest
 ingly\, we have found that siRNA mediated Myo19 knockdown cells exhibit a 
 reduction in the rate of cell migration measured using 2D in-vitro cell sc
 ratch assay. This phenotype is most likely robust in several cell lines th
 at we have explored. We have also begun to identify key signaling evens th
 at may be related to triggering mitochondrial motility to filopodia. These
  findings provide the basis for the direct involvement of Myo19 in various
  physiological process that are manifested by actin protrusions. 

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