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  1. Article ; Online: Common inhibitory serine sites phosphorylated by IRS-1 kinases, triggered by insulin and inducers of insulin resistance.

    Herschkovitz, Avia / Liu, Yan-Fang / Ilan, Erez / Ronen, Denise / Boura-Halfon, Sigalit / Zick, Yehiel

    The Journal of biological chemistry

    2018  Volume 293, Issue 19, Page(s) 7266

    Language English
    Publishing date 2018-05-11
    Publishing country United States
    Document type Journal Article ; Retraction of Publication
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.W118.003468
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Insulin stimulates PKCζ -mediated phosphorylation of insulin receptor substrate-1 (IRS-1): A self-attenuated mechanism to negatively regulate the function of IRS proteins.

    Liu, Yan-Fang / Paz, Keren / Herschkovitz, Avia / Alt, Addy / Tennenbaum, Tamar / Sampson, Sanford R / Ohba, Motoi / Kuroki, Toshio / LeRoith, Derek / Zick, Yehiel

    The Journal of biological chemistry

    2018  Volume 293, Issue 19, Page(s) 7264

    Language English
    Publishing date 2018-05-11
    Publishing country United States
    Document type Journal Article ; Retraction of Publication
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.W118.003466
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Common inhibitory serine sites phosphorylated by IRS-1 kinases, triggered by insulin and inducers of insulin resistance.

    Herschkovitz, Avia / Liu, Yan-Fang / Ilan, Erez / Ronen, Denise / Boura-Halfon, Sigalit / Zick, Yehiel

    publication RETRACTED

    The Journal of biological chemistry

    2007  Volume 282, Issue 25, Page(s) 18018–18027

    Abstract: The Insulin Receptor Substrate (IRS) proteins are key players in insulin signal transduction and are the best studied targets of the insulin receptor. Ser/Thr phosphorylation of IRS proteins negatively modulates insulin signaling; therefore, the ... ...

    Abstract The Insulin Receptor Substrate (IRS) proteins are key players in insulin signal transduction and are the best studied targets of the insulin receptor. Ser/Thr phosphorylation of IRS proteins negatively modulates insulin signaling; therefore, the identification of IRS kinases and their target Ser phosphorylation sites is of physiological importance. Here we show that in Fao rat hepatoma cells, the IkappaB kinase beta (IKKbeta) is an IRS-1 kinase activated by selected inducers of insulin resistance, including sphingomyelinase, ceramide, and free fatty acids. Moreover, IKKbeta shares a repertoire of seven potential target sites on IRS-1 with protein kinase C zeta (PKCzeta), an IRS-1 kinase activated both by insulin and by inducers of insulin resistance. We further show that mutation of these seven sites (Ser-265, Ser-302, Ser-325, Ser-336, Ser-358, Ser-407, and Ser-408) confers protection from the action of IKKbeta and PKCzeta when they are overexpressed in Fao cells or primary hepatocytes. This enables the mutated IRS proteins to better propagate insulin signaling. These findings suggest that insulin-stimulated IRS kinases such as PKCzeta overlap with IRS kinases triggered by inducers of insulin resistance, such as IKKbeta, to phosphorylate IRS-1 on common Ser sites.
    MeSH term(s) Animals ; Fatty Acids, Nonesterified/metabolism ; Hepatocytes/metabolism ; Humans ; I-kappa B Kinase/metabolism ; Insulin/metabolism ; Insulin Receptor Substrate Proteins ; Insulin Resistance ; Male ; Phosphoproteins/chemistry ; Phosphoproteins/physiology ; Phosphorylation ; Protein Kinase C/metabolism ; Rats ; Rats, Wistar ; Serine/chemistry ; Sphingomyelin Phosphodiesterase/metabolism
    Chemical Substances Fatty Acids, Nonesterified ; IRS1 protein, human ; Insulin ; Insulin Receptor Substrate Proteins ; Irs1 protein, rat ; Phosphoproteins ; Serine (452VLY9402) ; protein kinase C zeta (EC 2.7.11.1) ; I-kappa B Kinase (EC 2.7.11.10) ; Protein Kinase C (EC 2.7.11.13) ; Sphingomyelin Phosphodiesterase (EC 3.1.4.12)
    Language English
    Publishing date 2007-04-19
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Retracted Publication
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.M610949200
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Demyelination arrest and remyelination induced by glatiramer acetate treatment of experimental autoimmune encephalomyelitis.

    Aharoni, Rina / Herschkovitz, Avia / Eilam, Raya / Blumberg-Hazan, Michal / Sela, Michael / Bruck, Wolfgang / Arnon, Ruth

    Proceedings of the National Academy of Sciences of the United States of America

    2008  Volume 105, Issue 32, Page(s) 11358–11363

    Abstract: The interplay between demyelination and remyelination is critical in the progress of multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). In the present study, we explored the capacity of glatiramer acetate (GA, ... ...

    Abstract The interplay between demyelination and remyelination is critical in the progress of multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). In the present study, we explored the capacity of glatiramer acetate (GA, Copaxone) to affect the demyelination process and/or lead to remyelination in mice inflicted by chronic EAE, using both scanning electron microscopy and immunohistological methods. Spinal cords of untreated EAE mice revealed substantial demyelination accompanied by tissue destruction and axonal loss. In contrast, in spinal cords of GA-treated mice, in which treatment started concomitantly with disease induction (prevention), no pathology was observed. Moreover, when treatment was initiated after the appearance of clinical symptoms (suppression) or even in the chronic disease phase (delayed suppression) when substantial demyelination was already manifested, it resulted in a significant decrease in the pathological damage. Detection of oligodendrocyte progenitor cells (OPCs) expressing the NG2 or O4 markers via colocalization with the proliferation marker BrdU indicated their elevated levels in spinal cords of GA-treated mice. The mode of action of GA in this system is attributed to increased proliferation, differentiation, and survival of OPCs along the oligodendroglial maturation cascade and their recruitment into injury sites, thus enhancing repair processes in situ.
    MeSH term(s) Animals ; Antigens/biosynthesis ; Antigens, Differentiation/biosynthesis ; Axons/metabolism ; Axons/ultrastructure ; Cell Proliferation/drug effects ; Chronic Disease ; Encephalomyelitis, Autoimmune, Experimental/chemically induced ; Encephalomyelitis, Autoimmune, Experimental/drug therapy ; Encephalomyelitis, Autoimmune, Experimental/metabolism ; Encephalomyelitis, Autoimmune, Experimental/pathology ; Encephalomyelitis, Autoimmune, Experimental/prevention & control ; Glatiramer Acetate ; Immunosuppressive Agents/pharmacology ; Mice ; Microscopy, Electron, Scanning ; Multiple Sclerosis/chemically induced ; Multiple Sclerosis/drug therapy ; Multiple Sclerosis/metabolism ; Multiple Sclerosis/pathology ; Myelin Sheath/metabolism ; Myelin Sheath/ultrastructure ; Oligodendroglia/metabolism ; Oligodendroglia/ultrastructure ; Peptides/pharmacology ; Proteoglycans/biosynthesis ; Recovery of Function/drug effects ; Spinal Cord/metabolism ; Spinal Cord/ultrastructure ; Stem Cells/metabolism ; Stem Cells/ultrastructure
    Chemical Substances Antigens ; Antigens, Differentiation ; Immunosuppressive Agents ; Peptides ; Proteoglycans ; chondroitin sulfate proteoglycan 4 ; Glatiramer Acetate (5M691HL4BO)
    Language English
    Publishing date 2008-08-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.0804632105
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1148: Show issues Location:
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  5. Article: Demyelination arrest and remyelination induced by glatiramer acetate treatment of experimental autoimmune encephalomyelitis

    Aharoni, Rina / Herschkovitz, Avia / Eilam, Raya / Blumberg-Hazan, Michal / Sela, Michael / Bruck, Wolfgang / Arnon, Ruth

    Proceedings of the National Academy of Sciences of the United States of America. 2008 Aug. 12, v. 105, no. 32

    2008  

    Abstract: The interplay between demyelination and remyelination is critical in the progress of multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). In the present study, we explored the capacity of glatiramer acetate (GA, ... ...

    Abstract The interplay between demyelination and remyelination is critical in the progress of multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). In the present study, we explored the capacity of glatiramer acetate (GA, Copaxone) to affect the demyelination process and/or lead to remyelination in mice inflicted by chronic EAE, using both scanning electron microscopy and immunohistological methods. Spinal cords of untreated EAE mice revealed substantial demyelination accompanied by tissue destruction and axonal loss. In contrast, in spinal cords of GA-treated mice, in which treatment started concomitantly with disease induction (prevention), no pathology was observed. Moreover, when treatment was initiated after the appearance of clinical symptoms (suppression) or even in the chronic disease phase (delayed suppression) when substantial demyelination was already manifested, it resulted in a significant decrease in the pathological damage. Detection of oligodendrocyte progenitor cells (OPCs) expressing the NG2 or O4 markers via colocalization with the proliferation marker BrdU indicated their elevated levels in spinal cords of GA-treated mice. The mode of action of GA in this system is attributed to increased proliferation, differentiation, and survival of OPCs along the oligodendroglial maturation cascade and their recruitment into injury sites, thus enhancing repair processes in situ.
    Language English
    Dates of publication 2008-0812
    Size p. 11358-11363.
    Publishing place National Academy of Sciences
    Document type Article
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    Database NAL-Catalogue (AGRICOLA)

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  6. Article: Serine phosphorylation proximal to its phosphotyrosine binding domain inhibits insulin receptor substrate 1 function and promotes insulin resistance.

    Liu, Yan-Fang / Herschkovitz, Avia / Boura-Halfon, Sigalit / Ronen, Denise / Paz, Keren / Leroith, Derek / Zick, Yehiel

    Molecular and cellular biology

    2004  Volume 24, Issue 21, Page(s) 9668–9681

    Abstract: Ser/Thr phosphorylation of insulin receptor substrate (IRS) proteins negatively modulates insulin signaling. Therefore, the identification of serine sites whose phosphorylation inhibit IRS protein functions is of physiological importance. Here we mutated ...

    Abstract Ser/Thr phosphorylation of insulin receptor substrate (IRS) proteins negatively modulates insulin signaling. Therefore, the identification of serine sites whose phosphorylation inhibit IRS protein functions is of physiological importance. Here we mutated seven Ser sites located proximal to the phosphotyrosine binding domain of insulin receptor substrate 1 (IRS-1) (S265, S302, S325, S336, S358, S407, and S408) into Ala. When overexpressed in rat hepatoma Fao or CHO cells, the mutated IRS-1 protein in which the seven Ser sites were mutated to Ala (IRS-1(7A)), unlike wild-type IRS-1 (IRS-1(WT)), maintained its Tyr-phosphorylated active conformation after prolonged insulin treatment or when the cells were challenged with inducers of insulin resistance prior to acute insulin treatment. This was due to the ability of IRS-1(7A) to remain complexed with the insulin receptor (IR), unlike IRS-1(WT), which underwent Ser phosphorylation, resulting in its dissociation from IR. Studies of truncated forms of IRS-1 revealed that the region between amino acids 365 to 430 is a main insulin-stimulated Ser phosphorylation domain. Indeed, IRS-1 mutated only at S408, which undergoes phosphorylation in vivo, partially maintained the properties of IRS-1(7A) and conferred protection against selected inducers of insulin resistance. These findings suggest that S408 and additional Ser sites among the seven mutated Ser sites are targets for IRS-1 kinases that play a key negative regulatory role in IRS-1 function and insulin action. These sites presumably serve as points of convergence, where physiological feedback control mechanisms, which are triggered by insulin-stimulated IRS kinases, overlap with IRS kinases triggered by inducers of insulin resistance to terminate insulin signaling.
    MeSH term(s) Adenoviridae/genetics ; Animals ; Binding Sites ; Cell Line ; Cricetinae ; Enzyme Activation ; Gene Expression Regulation, Viral ; Genes, myc/genetics ; Humans ; Insulin/pharmacology ; Insulin Receptor Substrate Proteins ; Insulin Resistance ; Mice ; Mitogen-Activated Protein Kinases/metabolism ; Mutation/genetics ; Phosphoproteins/antagonists & inhibitors ; Phosphoproteins/genetics ; Phosphoproteins/metabolism ; Phosphorylation ; Phosphoserine/metabolism ; Phosphotyrosine/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Serine/genetics ; Serine/metabolism
    Chemical Substances IRS1 protein, human ; Insulin ; Insulin Receptor Substrate Proteins ; Irs1 protein, mouse ; Irs1 protein, rat ; Phosphoproteins ; Proto-Oncogene Proteins ; Phosphoserine (17885-08-4) ; Phosphotyrosine (21820-51-9) ; Serine (452VLY9402) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2004-11
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 779397-2
    ISSN 1098-5549 ; 0270-7306
    ISSN (online) 1098-5549
    ISSN 0270-7306
    DOI 10.1128/MCB.24.21.9668-9681.2004
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

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