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Lipid helps cell wall protein fold

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General fitness, health and nutrition
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18 July 2005
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  1. Beyond genes - Lipid helps cell wall protein fold into proper shape
    17 Jul 2005

    A protein that provides a vital passage through a bacterium's outer
    cell wall will misfold and malfunction if that wall is built of the
    'wrong' material, scientists at The University of Texas Medical School
    at Houston report in a finding that has long-term implications for
    understanding diseases caused by misfolded proteins such as cystic
    fibrosis, Alzheimer's disease, and mad cow disease.

    The paper in today's Journal of Biological Chemistry by Professor of
    Biochemistry and Molecular Biology William Dowhan, Ph.D., and
    colleagues shows that phospholipids, which make up the permeable
    barrier of cell membranes, play a direct role in the folding of
    membrane proteins - proteins that penetrate the membrane or bind to
    either side of it.

    "What we've demonstrated again is that it's not just a membrane
    protein's genetically determined sequence that dictates how it folds so
    that it can function properly. Its lipid environment also plays a
    role," Dowhan said. "People used to assume that specific lipids made no
    difference."

    In the JBC paper, Dowhan and colleagues looked at how a protein called
    GabP, which transports an amino acid across the membrane of the
    bacterium E. coli, is affected by the presence of a phospholipid named
    phosphatidylethanolamine, or PE for short.

    Phospholipids, unlike their fatty acid and cholesterol cousins, include
    a phosphate group that spurs them to form a bilayer with water-friendly
    outer layers sandwiching an impermeable water-unfriendly inner layer
    that defines the outer surface of cells. Transport of nutrients and
    waste material across the cell membrane is then governed by the
    specific proteins associated with it.

    In a strain of E. coli lacking PE, the GabP protein misfolded, with two
    areas of the protein inverting from their normal structure. The
    PE-lacking protein's amino acid transfer rate plummeted to nearly zero,
    falling 99 percent compared to the transfer rate in unaltered E. coli
    with PE.

    GabP is the third membrane protein that Dowhan and colleagues have
    shown to be affected by the presence of PE.

    The team is using the E. coli model to discover how all proteins fold
    in the membrane, not just transport proteins such as GabP but also
    biosynthetic proteins that manufacture complex compounds such as
    proteins and fats out of simple compounds.

    "The next goal now that we've defined the phenomenon is to get into the
    specifics, find the mechanisms by which these proteins fold. What part
    of the protein interacts with the lipid, and what part of the lipid
    with the protein?" said Dowhan, who holds the John S. Dunn Sr. Chair in
    Biochemistry and Molecular Biology and is on the Graduate School of
    Biomedical Sciences faculty.

    Understanding the molecular basis for membrane protein folding will
    help researchers address serious diseases caused by misfolded proteins.
    "In cystic fibrosis, Alzheimer's disease and mad cow disease, the
    dysfunctional proteins are associated with membranes," Dowhan said.

    Membrane proteins make up 30 percent of known proteins. Dowhan
    estimates another 40 percent are loosely tied to membranes. "So you are
    looking at possibly 70 percent of biology occurring at or in a lipid
    membrane surface," Dowhan said.

    Membranes and their surface proteins are accessible targets for
    pharmaceuticals, and most drugs target either membrane proteins on
    human cells or the membranes of pathogens.

    Co-authors of the JBC paper with senior author Dowhan are first author
    Wei Zhang, Ph.D., a former graduate student who is now a post-doctoral
    fellow at Stanford University, and post-doctoral fellow Heidi Campbell,
    Ph.D., of the UT Medical School Department of Biochemistry, and
    Molecular Biology, and Steven King, Ph.D, associate professor,
    Department of Integrative Biosciences at Oregon Health & Science
    University.

    Dowhan recently was granted a MERIT award by the National Institute of
    General Medical Sciences of the National Institutes of Health.

    These rare awards provide long-term grant support for scientists whose
    research competence and productivity are distinctly superior and who
    are likely to continue to perform in an outstanding manner, the NIGMS
    notes.

    MERIT (Method to Extend Research in Time) status essentially gives
    Dowhan a 10-year renewal to 2015 on his longstanding NIGMS grant
    "Structure and Function of Membrane Proteins" by providing back-to-back
    five-year grants of $2.4 million apiece.

    In April, Dowhan received the prestigious American Society for
    Biochemistry and Molecular Biology Avanti Award in Lipids.

    Scott Merville
    [email hidden]
    713-500-3042
    University of Texas Health Science Center at Houston
    http://www.uthouston.edu

    --------------------------------------------------------------------------------

    Who loves ya.
    Tom

    Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com
    Man Is A Herbivore!
    http://pages.ivillage.com/ironjustice/manisaherbivore
    DEAD PEOPLE WALKING
    http://pages.ivillage.com/ironjustice/deadpeoplewalking

  2. Typical nothing abstract. What are they saying? Nothing that plenty
    of people already know. The actions of fatty acids in an aqueous
    environment are obvious - basic science. They speak as if there is
    some sort of mystery here. PE is likely being damaged by lipid
    peroxidation, and then they can't help the proteins fold correctly.
    That is the biggest problem. Otherwise, the body can take care of
    itself - if it didn't, we wouldn't be here. The new development is the
    massive free radical damage from "modern" diets. The fact that they
    don't mention free radical damage is evidence for why these types of
    "experts" can't "cure" any "diseases." They are clueless, studying the
    wrong things in the wrong ways.

  3. As you've been told .. before ..

    Proof .. is .. forthcoming ..

    they have NOW .. narrowed it DOWN .. to .. phosphatidylethanolamine ..

    NOW .. they move ONTO .. why it is BEING .. oxidized .. SELECTIVELY ..
    and BY .. what ..

    My guess it will be .. iron ..

    Who loves ya.
    Tom
    Jesus Was A Vegetarian!
    http://jesuswasavegetarian.7h.com
    Man Is A Herbivore!
    http://pages.ivillage.com/ironjustice/manisaherbivore
    DEAD PEOPLE WALKING
    http://pages.ivillage.com/ironjustice/deadpeoplewalking

  4. Quoted message said:

    As you've been told .. before ..

    Proof .. is .. forthcoming ..

    they have NOW .. narrowed it DOWN .. to .. phosphatidylethanolamine ..

    NOW .. they move ONTO .. why it is BEING .. oxidized .. SELECTIVELY ..
    and BY .. what ..

    My guess it will be .. iron ..

    Who loves ya.
    Tom

    <<snip>>
    demonstrating that phosphatidylethanolamine (PE) was most sensitive to
    peroxidation
    <<snip>>

    J Neurochem. 1996 Jan;66(1):355-61. Related Articles, Links

    Direct measurement of lipid hydroperoxides in iron-dependent spinal neuronal
    injury.

    Zhang JR, Scherch HM, Hall ED.

    CNS Diseases Research, Upjohn Company, Kalamazoo, Michigan 49001, USA.

    The relationship between iron-dependent fetal mouse spinal cord neuron injury
    and the generation of endogenous lipid hydroperoxides (LOOHs) has been
    investigated. Cultured spinal cord neurons were incubated with ferrous iron
    (3-200 microM). Cell viability was measured in terms of the uptake of alpha-
    [methyl-3H]aminoisobutyric acid ([3H]AIB). Both endogenously and iron-
    generated LOOH, i.e., free fatty acid hydroperoxide (FFAOOH),
    phosphatidylethanolamine hydroperoxide (PEOOH), and phosphatidylcholine
    hydroperoxide (PCOOH), were measured directly by an HPLC-chemiluminescence
    (HPLC-CL) assay. The FFAOOH, PEOOH, and PCOOH levels in neurons incubated
    with 200 microM Fe2+ for 40 min were, respectively, 22-, 158-, and sevenfold
    higher than those in non-iron-exposed cultures, demonstrating that
    phosphatidylethanolamine (PE) was most sensitive to peroxidation. The dose-
    response and time course of Fe(2+)-induced generation of these LOOHs were
    also established. In both experiments, the LOOH levels were correlated
    directly with loss of neuronal viability, suggesting strongly a direct
    relationship between lipid peroxidation and cell injury. On examination of
    the time course of the LOOH generation, an immediate increase in PEOOH and
    PCOOH levels with only 30 s of Fe2+ incubation was observed. In contrast, a
    lag phase in the increase in FFAOOH level (2 min after Fe2+ addition)
    suggested a delay in the activation of phospholipase A2 (PLA2) required for
    the hydrolysis and generation of FFAOOH. This culture system provides an
    excellent model for screening antioxidant neuroprotective compounds with
    regard to their ability to protect against iron-dependent peroxidative injury
    and the relationship of the neuroprotection to inhibition of lipid
    peroxidation and/or PLA2.

    PMID: 8522975 [PubMed - indexed for MEDLINE]

    ------------------------------------------------------------------------------
    --

    Quoted message said:

    Jesus Was A Vegetarian!
    http://jesuswasavegetarian.7h.com
    Man Is A Herbivore!
    http://pages.ivillage.com/ironjustice/manisaherbivore
    DEAD PEOPLE WALKING
    http://pages.ivillage.com/ironjustice/deadpeoplewalking

    --
    Message posted via MedKB.com
    http://www.medkb.com/Uwe/Forums.aspx/nutrition/200507/1

  5. Do your realize that iron can be a catalyst, but that there needs to be
    sufficient biochemical activity for it to be dangerous? If you put
    iron in a vacuum-sealed transparent box, what will it do? Nothing.
    The Asian study that was posted here made that clear. They have high
    iron levels, yet a much lower incidence of the "diseases" associated
    with such levels in Western nations, due to a diet that generates
    massive free radical activity.

  6. montygram said:

    Typical nothing abstract.

    It's not an abstract.

    Quoted message said:

    What are they saying? Nothing that plenty
    of people already know.

    You don't know what they're saying, but you're confident plenty of
    people already know it? I think the problem is it's about lipid
    bilayers and your brain just switches off when they're brought up.

    Quoted message said:

    The actions of fatty acids in an aqueous
    environment are obvious - basic science.

    And irrelevant to this paper.

    Quoted message said:

    They speak as if there is
    some sort of mystery here. PE is likely being damaged by lipid
    peroxidation, and then they can't help the proteins fold correctly.

    Either you didn't read it or just don't have a clue. It's nothing to do
    with the fatty side-chains. It's the phospho-ethanolamine head group
    that's important.

    MattLB

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