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  • Researchers Solve Killer Protein’s “Crime” | Newswire
    System In their latest research the Rockefeller researchers demonstrate that Reaper triggers DIAP1 to undergo a process known as auto ubiquitination which essentially amounts to protein suicide Ubiquitination like its name implies takes place in every cell at all times and is the body s main system for eliminating protein waste proteins called ubiquitin ligases such as DIAP1 tag proteins that are no longer needed by the cell with a small molecule called ubiquitin which then signals a large protein complex called the proteasome to essentially chew it up and spit it out Auto ubiquitination occurs when a protein marks itself for destruction But over the past few years scientists have come to realize that ubiquitination is much more than a garbage disposal system rather it is one of the cell s principal strategies for regulating the amount of a given protein in a cell Moreover a malfunctioning ubiquitination system can lead to several diseases including cancer autoimmune disease and such neurodegenerative diseases as Parkinson s The latest finding that Reaper stimulates DIAP1 to ubiquitinate itself not only represents a novel cell death mechanism but marks a first in the field of ubiquitination For the first time we have shown that another protein Reaper enhances the activity of a ubiquitinating ligase DIAP1 says Ryoo The rate of DIAP1 ubiquitination is not constant but is actively stimulated in cells that are fated to die Gas and Brake Model of Cell Death The protein DIAP1 normally keeps a tight leash on the deadly caspases red shown above outside of the nuclei green of developing fly embryo cells But when the protein Reaper stimulates DIAP1 to self destruct the caspases are released and natural cell death ensues The primary executioners in programmed cell death are proteins called caspases These are the proteins that wreak havoc on a cell and eventually kill it Other proteins which Steller calls the gas signal a cell to activate caspases when its time to die But in a healthy cell the presence of active caspases is not enough to induce cell death these deadly molecules are kept on a tight leash by the IAPs or as Steller calls them the brakes on death Consequently before cell death can occur these brakes must be released This is the job of the Reaper family of proteins which includes Reaper Hid and Grim and which Steller discovered in 1994 Reaper is like a molecular switch that triggers cell death by inactivating a pro life IAP protein DIAP1 In living cells DIAP1 is abundant and prevents apoptosis says Ryoo But in cells that are doomed to die Reaper inactivates DIAP1 which then leads to the release of the caspases Reaper Hid and Grim are like the keys that unlock the chains of deadly caspases adds Steller But until now scientists did not know the precise mechanism by which the Reaper family of proteins inactivated the IAPs or in other words released the breaks on death The new Rockefeller research is the first

    Original URL path: http://newswire.rockefeller.edu/2002/06/07/researchers-solve-killer-proteins-crime/ (2016-02-13)
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  • Cells on the Verge of Suicide | Newswire
    brakes on death and this in turn results in an unleashing of toxic proteins called caspases In the article Steller and colleagues outline the entire molecular pathway by which a population of neuron cells in the brains of developing fruit flies communicate a message of survival to a different class of neighboring cells in the brain called glial cells The research was conducted at the Massachusetts Institute of Technology in Cambridge Mass and the Weizmann Institute of Science in Israel Steller says that these findings may serve as a model for what takes place in human brains and possibly in other parts of the body such as our immune system skin liver and colon where this type of programmed cell death naturally occurs throughout life The human brain as well as the fly brain consists of two main types of cells neurons and glial cells Neurons are the primary cells of the brain and are responsible for a host of essential body functions including learning memory behavior and sensory perception Glial cells on the other hand play a more backseat role to neurons acting mainly to support their activities During development billions of both cell types arise but only a small percentage actually survive to form the adult brain The rest undergo a type of cell suicide known as apoptosis pronounced a pop TOE sis from the Greek word for falling away This natural cell death occurs throughout the body both during development as a means to sculpt critical organs and tissues and in adults as a housekeeping function that eliminates potentially harmful cells Just how cells know whether to survive or perish has been the subject of intense study for nearly 50 years In the last decade researchers have learned that during development virtually all cells require specific external signals called survival factors or trophic factors which are secreted from neighboring cells to survive Those that do not receive the trophic signals commit suicide by default That is cells have to compete for trophic signals in order to survive This social control theory of cell survival explains why no one cell type outnumbers another says Steller The body has essentially figured out a way to keep its cell numbers in check The brain s trophic survival signals work by suppressing a cell s cell death machinery which includes Grim Reaper and Hid and a family of enzymes called caspases Normally caspases which are the key executioners are locked up by other proteins which I refer to as the brakes on death says Steller who discovered the Reaper family in 1994 But in order to get cells to self destruct these brakes have to be released and that s the job of Reaper Hid and Grim Like keys unlocking the door to a dangerous beast restrained behind it they activate other proteins called caspases to chop up all sorts of proteins and death ensues Although scientists understood the mechanics of this cell suicide process they did not know how it

    Original URL path: http://newswire.rockefeller.edu/2002/02/01/cells-on-the-verge-of-suicide/ (2016-02-13)
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  • Researchers Shed Light on How Cells Commit Suicide | Newswire
    and infertility occur when there is an excess of cell death Cowburn collaborated with Stanley Korsmeyer M D and Curt A Milliman B S at Washington University School of Medicine Korsmeyer now at the Dana Farber Cancer Institute at Harvard Medical School has spent the last several years studying a family of proteins called Bcl 2 which he and others has shown to be involved in the cell death process Some members of the protein family induce cell death and are known as proapoptotic agents while others called antiapoptotic agents prevent it The structure solved known as Bid Bcl 2 interacting domain is a proapoptotic member of the Bcl 2 protein family Recently Korsmeyer s group and others showed that Bid which is normally inactive becomes active when cleaved or chopped up by an enzyme called a caspase The truncated form of Bid designated tBid travels to the cell s power house the mitochondria wreaking havoc with the cellular machinery and causing the cell to die First author James McDonnell Ph D and co author David Fushman Ph D with Cowburn used a technique called nuclear magnetic resonance NMR to study the Bcl 2 proteins NMR is a technique for observing molecules as they float in solution much like their natural environment in the living cell providing dynamic views of the molecules and their functions The structure is a complex packing of several helices against each other The site of cutting by the enzyme surprisingly resides in a long unstructured loop Modeling how the cut molecule looks suggests that the product is much more hydrophobic and less charged possibly making it suitable to be a membrane pore former in the mitochondria The solution NMR structure confirms the earlier observation Korsmeyer and his colleagues made using biochemical techniques and provides a

    Original URL path: http://newswire.rockefeller.edu/1999/03/05/researchers-shed-light-on-how-cells-commit-suicide/ (2016-02-13)
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  • Bcl-2 | Newswire
    of a moleculethat regulates programmed cell death a critical process importantfor many diseases including cancer heart disease and autoimmunity The structure reported in the March 5 issue of the journal Cell provides a model for developing compounds to switch cell suicideon or off to treat these diseases More Tags Bcl 2 David Cowburn programmed cell death Search for Categories Science News Awards and Honors Campus News Grants Gifts Topics Video

    Original URL path: http://newswire.rockefeller.edu/tag/bcl-2/ (2016-02-13)
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  • Shai Shaham and Sean Brady receive promotions | Newswire
    is the type of cell death on which researchers primarily focus It is therefore exciting to discover a new program that may be similarly conserved The Shaham lab has also been adding new insights to the topic of glial cells highly abundant nervous system cells that have historically been less explored than neurons Glia were thought to function solely as the workhorses that brought nutrients to and cleaned up after neurons but the Shaham lab has shown that glia are essential for neural development promoting axon outgrowth and dendrite extension The lab has also uncovered morphology independent roles for glia in sensory neuron function showing that animals lacking glia exhibit profound sensory deficits Recent research has centered on the communication between glia and neurons at the synapse and the role of glia in regulating the function of synaptic receptors Shaham who was born in Israel received his A B degree in biochemistry and a minor in mathematics from Columbia University in 1989 At the Massachusetts Institute of Technology he studied apoptotic cell death in the lab of Robert Horvitz and graduated with a Ph D in biology in 1995 After postdoctoral studies at the University of California San Francisco with Ira Herskowitz and Cori Bargmann Shaham was hired at Rockefeller as assistant professor in 2001 and promoted to associate professor in 2007 In 2010 Shaham received an NIH Director s Transformative Research Award and in 2009 he won a Blavatnik Award for Young Scientists a highly regarded award for early career researchers He also received a Klingenstein Fellowship Award in the Neurosciences and a Breast Cancer Alliance Masin Young Investigator Award and was named a scholar of both the Rita Allen Foundation and the Sidney Kimmel Foundation for Cancer Research Sean Brady head of the Laboratory of Genetically Encoded Small Molecules Sean Brady who joined the university in 2006 is interested in the discovery of new genetically encoded small molecules from bacterial sources chemicals that may be useful for the study of life or that may play a role in the development of new pharmaceuticals Since launching his laboratory six years ago Brady and his collaborators have shown that it is possible to use uncultured bacteria principally bacteria harvested from soil as a source of new small molecules and that these molecules are biologically active There s a lot of chemistry in these bacteria but because they cannot be grown in the laboratory much of it has been inaccessible says Brady We ve worked to develop tools that allow us to characterize and evaluate the natural products produced by a wide range of unstudied bacteria and we re now focused on screening for natural products that are the most relevant Because uncultured bacteria vastly outnumber their cultured counterparts they represent one of the largest remaining pools of unexplored genetic diversity and the chemicals they produce could potentially be the basis for new antibiotics anti fungal agents or anti cancer drugs to name a few Rather than approach nature with specific

    Original URL path: http://newswire.rockefeller.edu/2012/09/26/shai-shaham-and-sean-brady-receive-promotions/ (2016-02-13)
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  • Sean Brady | Newswire
    Shaham and Sean Brady receive promotions Shaham head of the Laboratory of Developmental Genetics studies the control of programmed cell death during animal development and the roles of glial cells in nervous system development and function He has been awarded tenure and promoted to professor Brady head of the Laboratory of Genetically Encoded Small Molecules looks for new genetically encoded small molecules from bacterial sources chemicals that may play a role in the development of new pharmaceuticals He has been promoted to associate professor More Tags Sean Brady Shai Shaham October 22 2007 Awards and Honors Sean Brady named 2007 Beckman Young investigator Chemical biologist Sean Brady head of Rockefeller University s Laboratory of Genetically Encoded Small Molecules is recognized for his ongoing work on the therapeutic potential of naturally occurring small molecules More Tags Beckman Young Investigator Sean Brady May 30 2006 Campus News Natural products chemist to become Rockefeller s newest lab head Following a yearlong search process involving an applicant pool of close to 700 candidates Rockefeller University President Paul Nurse has announced that Sean Brady a chemical biologist with a background in organic chemistry microbiology and plant biology will become assistant professor and head of laboratory

    Original URL path: http://newswire.rockefeller.edu/tag/sean-brady/ (2016-02-13)
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  • Scientists show how a neuron gets its shape | Newswire
    I thought that you would build a brain just like you would a house says Heiman The cell would measure the distance between its cell body and its target and then specify a dendrite of that length Now I m not thinking about that kind of physical map at all I think of a connectivity map where what s programmed are these connections among neurons and between neurons and their anchoring points Since they were interested in how neurons get their shapes Heiman and Shaham used a chemical to randomly mutate genes and then screened through thousands of animals for ones whose neurons were shaped abnormally They specifically looked at a group of 12 sensory neurons whose dendritic tips converge at the worm s nose in a sensory organ called the amphid These dendritic tips collect information from the outside environment and give the worm cues on how to react to it Two genes called dex 1 and dyf 7 caught their attention If the animals had a mutation in either one of these genes Heiman and Shaham saw that even though the cell migrated normally away from the tip of the nose the dendrite didn t stay anchored Instead it dragged along behind the cell body resulting in an abnormally short dendrite When they looked at the function of the proteins the researchers found that they form a matrix to which the dendrites are anchored Without the matrix to anchor the neuron the dendrites didn t form properly The two proteins it turns out are very similar to proteins that anchor the hair cells that detect sound waves in the human ear That was our second surprise says Heiman That there is this evolutionary relationship between a sensory organ in a worm and a sensory organ in humans In

    Original URL path: http://newswire.rockefeller.edu/2009/04/02/scientists-show-how-a-neuron-gets-its-shape/ (2016-02-13)
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  • Without glial cells, animals lose their senses | Newswire
    Maya Tevlin worked with a structure called the amphid a sensory organ in the Caenorhabditis elegans nervous system that contains glia and neurons Of the organ s 12 neurons four are completely ensheathed by glia and eight are partially ensheathed with sensory endings exposed to the outside environment via the worm s nose To see what glia do for these neurons Bacaj removed the glia and observed the effect on the neurons shape their ability to generate behavior when exposed to odors and temperatures and their ability to absorb certain dyes The results were striking The absence of glia affected at least one of these three properties in each of the neurons suggesting that glia not only regulate all of these properties but that they specifically regulate them in different neurons In the absence of glia for example the sensory endings of the ensheathed neurons lost their intricate branch like structure shriveling into nubs However the partially ensheathed neurons retained their normal shape despite their inability to respond to stimuli in their environment Instead of finding their perfect temperature the worms kept crawling toward warmer and warmer regions says Bacaj Also they didn t avoid odors they didn t like and weren t drawn to odors that they did like suggesting that the neurons could not coordinate an appropriate behavioral response It s a new layer of complexity that was never described before says Shaham To get a molecular handle on how glia regulate the functions of neurons Shaham Tevlin and Bacaj looked at which proteins are expressed more in glial cells than in any other cell in C elegans They found that one of these proteins called FIG 1 was exclusively expressed in glia surrounding the amphid sensory organ and its sister organ in the tail When the glia

    Original URL path: http://newswire.rockefeller.edu/2008/11/03/without-glial-cells-animals-lose-their-senses/ (2016-02-13)
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