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  1. Artikel ; Online: The orally bioavailable GSPT1/2 degrader SJ6986 exhibits in vivo efficacy in acute lymphoblastic leukemia.

    Chang, Yunchao / Keramatnia, Fatemeh / Ghate, Pankaj S / Nishiguchi, Gisele / Gao, Qingsong / Iacobucci, Ilaria / Yang, Lei / Chepyala, Divyabharathi / Mishra, Ashutosh / High, Anthony A / Goto, Hiroaki / Akahane, Koshi / Peng, Junmin / Yang, Jun J / Fischer, Marcus / Rankovic, Zoran / Mullighan, Charles G

    Blood

    2023  Band 142, Heft 7, Seite(n) 629–642

    Abstract: Advancing cure rates for high-risk acute lymphoblastic leukemia (ALL) has been limited by the lack of agents that effectively kill leukemic cells, sparing normal hematopoietic tissue. Molecular glues direct the ubiquitin ligase cellular machinery to ... ...

    Abstract Advancing cure rates for high-risk acute lymphoblastic leukemia (ALL) has been limited by the lack of agents that effectively kill leukemic cells, sparing normal hematopoietic tissue. Molecular glues direct the ubiquitin ligase cellular machinery to target neosubstrates for protein degradation. We developed a novel cereblon modulator, SJ6986, that exhibits potent and selective degradation of GSPT1 and GSPT2 and cytotoxic activity against childhood cancer cell lines. Here, we report in vitro and in vivo testing of the activity of this agent in a panel of ALL cell lines and xenografts. SJ6986 exhibited similar cytotoxicity to the previously described GSPT1 degrader CC-90009 in a panel of leukemia cell lines in vitro, resulting in apoptosis and perturbation of cell cycle progression. SJ6986 was more effective than CC-90009 in suppressing leukemic cell growth in vivo, partly attributable to favorable pharmacokinetic properties, and did not significantly impair differentiation of human CD34+ cells ex vivo. Genome-wide CRISPR/Cas9 screening of ALL cell lines treated with SJ6986 confirmed that components of the CRL4CRBN complex, associated adaptors, regulators, and effectors were integral in mediating the action of SJ6986. SJ6986 is a potent, selective, orally bioavailable GSPT1/2 degrader that shows broad antileukemic activity and has potential for clinical development.
    Mesh-Begriff(e) Humans ; Child ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Antineoplastic Agents/chemistry ; Piperidones/therapeutic use ; Isoindoles/therapeutic use
    Chemische Substanzen CC-90009 ; Antineoplastic Agents ; Piperidones ; Isoindoles
    Sprache Englisch
    Erscheinungsdatum 2023-05-12
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2022017813
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: Development of Potent and Selective Janus Kinase 2/3 Directing PG-PROTACs.

    Alcock, Lisa J / Chang, Yunchao / Jarusiewicz, Jamie A / Actis, Marisa / Nithianantham, Stanley / Mayasundari, Anand / Min, Jaeki / Maxwell, Dylan / Hunt, Jeremy / Smart, Brandon / Yang, Jun J / Nishiguchi, Gisele / Fischer, Marcus / Mullighan, Charles G / Rankovic, Zoran

    ACS medicinal chemistry letters

    2022  Band 13, Heft 3, Seite(n) 475–482

    Abstract: Aberrant activation of the JAK-STAT signaling pathway has been implicated in the pathogenesis of a range of hematological malignancies and autoimmune disorders. Here we describe the design, synthesis, and characterization of JAK2/3 PROTACs utilizing a ... ...

    Abstract Aberrant activation of the JAK-STAT signaling pathway has been implicated in the pathogenesis of a range of hematological malignancies and autoimmune disorders. Here we describe the design, synthesis, and characterization of JAK2/3 PROTACs utilizing a phenyl glutarimide (PG) ligand as the cereblon (CRBN) recruiter. SJ10542 displayed high selectivity over GSPT1 and other members of the JAK family and potency in patient-derived ALL cells containing both JAK2 fusions and CRLF2 rearrangements.
    Sprache Englisch
    Erscheinungsdatum 2022-02-21
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ISSN 1948-5875
    ISSN 1948-5875
    DOI 10.1021/acsmedchemlett.1c00650
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: ZNF384 Fusion Oncoproteins Drive Lineage Aberrancy in Acute Leukemia.

    Dickerson, Kirsten M / Qu, Chunxu / Gao, Qingsong / Iacobucci, Ilaria / Gu, Zhaohui / Yoshihara, Hiroki / Backhaus, Emily A / Chang, Yunchao / Janke, Laura J / Xu, Beisi / Wu, Gang / Papachristou, Evangelia K / D'Santos, Clive S / Roberts, Kathryn G / Mullighan, Charles G

    Blood cancer discovery

    2022  Band 3, Heft 3, Seite(n) 240–263

    Abstract: ZNF384-rearranged fusion oncoproteins (FO) define a subset of lineage ambiguous leukemias, but their mechanistic role in leukemogenesis and lineage ambiguity is poorly understood. Using viral expression in mouse and human hematopoietic stem and ... ...

    Abstract ZNF384-rearranged fusion oncoproteins (FO) define a subset of lineage ambiguous leukemias, but their mechanistic role in leukemogenesis and lineage ambiguity is poorly understood. Using viral expression in mouse and human hematopoietic stem and progenitor cells (HSPC) and a Ep300::Znf384 knockin mouse model, we show that ZNF384 FO promote hematopoietic expansion, myeloid lineage skewing, and self-renewal. In mouse HSPCs, concomitant lesions, such as NRASG12D, were required for fully penetrant leukemia, whereas in human HSPCs, expression of ZNF384 FO drove B/myeloid leukemia, with sensitivity of a ZNF384-rearranged xenograft to FLT3 inhibition in vivo. Mechanistically, ZNF384 FO occupy a subset of predominantly intragenic/enhancer regions with increased histone 3 lysine acetylation and deregulate expression of hematopoietic stem cell transcription factors. These data define a paradigm for FO-driven lineage ambiguous leukemia, in which expression in HSPCs results in deregulation of lineage-specific genes and hematopoietic skewing, progressing to full leukemia in the context of proliferative stress.
    Significance: Expression of ZNF384 FO early in hematopoiesis results in binding and deregulation of key hematopoietic regulators, skewing of hematopoiesis, and priming for leukemic transformation. These results reveal the interplay between cell of origin and expression of ZNF384 FO to mediate lineage ambiguity and leukemia development. This article is highlighted in the In This Issue feature, p. 171.
    Mesh-Begriff(e) Animals ; Hematopoiesis/genetics ; Hematopoietic Stem Cells/metabolism ; Humans ; Leukemia, Myeloid, Acute/genetics ; Mice ; Oncogene Proteins, Fusion/genetics ; Trans-Activators/genetics ; Transcription Factors/genetics
    Chemische Substanzen Oncogene Proteins, Fusion ; Trans-Activators ; Transcription Factors ; ZNF384 protein, human
    Sprache Englisch
    Erscheinungsdatum 2022-02-15
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 3028898-8
    ISSN 2643-3249 ; 2643-3230
    ISSN (online) 2643-3249
    ISSN 2643-3230
    DOI 10.1158/2643-3230.BCD-21-0163
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Selective CK1α degraders exert antiproliferative activity against a broad range of human cancer cell lines.

    Nishiguchi, Gisele / Mascibroda, Lauren G / Young, Sarah M / Caine, Elizabeth A / Abdelhamed, Sherif / Kooijman, Jeffrey J / Miller, Darcie J / Das, Sourav / McGowan, Kevin / Mayasundari, Anand / Shi, Zhe / Barajas, Juan M / Hiltenbrand, Ryan / Aggarwal, Anup / Chang, Yunchao / Mishra, Vibhor / Narina, Shilpa / Thomas, Melvin / Loughran, Allister J /
    Kalathur, Ravi / Yu, Kaiwen / Zhou, Suiping / Wang, Xusheng / High, Anthony A / Peng, Junmin / Pruett-Miller, Shondra M / Daniels, Danette L / Urh, Marjeta / Shelat, Anang A / Mullighan, Charles G / Riching, Kristin M / Zaman, Guido J R / Fischer, Marcus / Klco, Jeffery M / Rankovic, Zoran

    Nature communications

    2024  Band 15, Heft 1, Seite(n) 482

    Abstract: Molecular-glue degraders are small molecules that induce a specific interaction between an E3 ligase and a target protein, resulting in the target proteolysis. The discovery of molecular glue degraders currently relies mostly on screening approaches. ... ...

    Abstract Molecular-glue degraders are small molecules that induce a specific interaction between an E3 ligase and a target protein, resulting in the target proteolysis. The discovery of molecular glue degraders currently relies mostly on screening approaches. Here, we describe screening of a library of cereblon (CRBN) ligands against a panel of patient-derived cancer cell lines, leading to the discovery of SJ7095, a potent degrader of CK1α, IKZF1 and IKZF3 proteins. Through a structure-informed exploration of structure activity relationship (SAR) around this small molecule we develop SJ3149, a selective and potent degrader of CK1α protein in vitro and in vivo. The structure of SJ3149 co-crystalized in complex with CK1α + CRBN + DDB1 provides a rationale for the improved degradation properties of this compound. In a panel of 115 cancer cell lines SJ3149 displays a broad antiproliferative activity profile, which shows statistically significant correlation with MDM2 inhibitor Nutlin-3a. These findings suggest potential utility of selective CK1α degraders for treatment of hematological cancers and solid tumors.
    Mesh-Begriff(e) Humans ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/chemistry ; Cell Line ; Neoplasms/drug therapy ; Proteolysis ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism
    Chemische Substanzen Antineoplastic Agents ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; CSNK1A1 protein, human (EC 2.7.11.1)
    Sprache Englisch
    Erscheinungsdatum 2024-01-16
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-024-44698-1
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Reduced inflammation accompanies diminished myelin damage and repair in the NG2 null mouse spinal cord

    Kucharova Karolina / Chang Yunchao / Boor Andrej / Yong Voon / Stallcup William B

    Journal of Neuroinflammation, Vol 8, Iss 1, p

    2011  Band 158

    Abstract: Abstract Background Multiple sclerosis (MS) is a demyelinating disease in which blood-derived immune cells and activated microglia damage myelin in the central nervous system. While oligodendrocyte progenitor cells (OPCs) are essential for generating ... ...

    Abstract Abstract Background Multiple sclerosis (MS) is a demyelinating disease in which blood-derived immune cells and activated microglia damage myelin in the central nervous system. While oligodendrocyte progenitor cells (OPCs) are essential for generating oligodendrocytes for myelin repair, other cell types also participate in the damage and repair processes. The NG2 proteoglycan is expressed by OPCs, pericytes, and macrophages/microglia. In this report we investigate the effects of NG2 on these cell types during spinal cord demyelination/remyelination. Methods Demyelinated lesions were created by microinjecting 1% lysolecithin into the lumbar spinal cord. Following demyelination, NG2 expression patterns in wild type mice were studied via immunostaining. Immunolabeling was also used in wild type and NG2 null mice to compare the extent of myelin damage, the kinetics of myelin repair, and the respective responses of OPCs, pericytes, and macrophages/microglia. Cell proliferation was quantified by studies of BrdU incorporation, and cytokine expression levels were evaluated using qRT-PCR. Results The initial volume of spinal cord demyelination in wild type mice is twice as large as in NG2 null mice. However, over the ensuing 5 weeks there is a 6-fold improvement in myelination in wild type mice, versus only a 2-fold improvement in NG2 null mice. NG2 ablation also results in reduced numbers of each of the three affected cell types. BrdU incorporation studies reveal that reduced cell proliferation is an important factor underlying NG2-dependent decreases in each of the three key cell populations. In addition, NG2 ablation reduces macrophage/microglial cell migration and shifts cytokine expression from a pro-inflammatory to anti-inflammatory phenotype. Conclusions Loss of NG2 expression leads to decreased proliferation of OPCs, pericytes, and macrophages/microglia, reducing the abundance of all three cell types in demyelinated spinal cord lesions. As a result of these NG2-dependent changes, the course of demyelination and remyelination in NG2 null mice differs from that seen in wild type mice, with both myelin damage and repair being reduced in the NG2 null mouse. These studies identify NG2 as an important factor in regulating myelin processing, suggesting that therapeutic targeting of the proteoglycan might offer a means of manipulating cell behavior in demyelinating diseases.
    Schlagwörter Inflammation ; myelin repair ; NG2 ablation ; oligodendrocyte progenitors ; pericytes ; macrophages ; Medicine (General) ; R5-920 ; Medicine ; R ; DOAJ:Medicine (General) ; DOAJ:Health Sciences ; Neurology. Diseases of the nervous system ; RC346-429 ; Neurosciences. Biological psychiatry. Neuropsychiatry ; RC321-571 ; Internal medicine ; RC31-1245 ; DOAJ:Neurology
    Thema/Rubrik (Code) 616
    Sprache Englisch
    Erscheinungsdatum 2011-11-01T00:00:00Z
    Verlag BioMed Central
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  6. Artikel ; Online: NG2 Proteoglycan Ablation Reduces Foam Cell Formation and Atherogenesis via Decreased Low-Density Lipoprotein Retention by Synthetic Smooth Muscle Cells.

    She, Zhi-Gang / Chang, Yunchao / Pang, Hong-Bo / Han, Wenlong / Chen, Hou-Zao / Smith, Jeffrey W / Stallcup, William B

    Arteriosclerosis, thrombosis, and vascular biology

    2016  Band 36, Heft 1, Seite(n) 49–59

    Abstract: Objectives: Obesity and hyperlipidemia are critical risk factors for atherosclerosis. Because ablation of NG2 proteoglycan in mice leads to hyperlipidemia and obesity, we investigated the impact of NG2 ablation on atherosclerosis in apoE null mice.: ... ...

    Abstract Objectives: Obesity and hyperlipidemia are critical risk factors for atherosclerosis. Because ablation of NG2 proteoglycan in mice leads to hyperlipidemia and obesity, we investigated the impact of NG2 ablation on atherosclerosis in apoE null mice.
    Approach and results: Immunostaining indicates that NG2 expression in plaque, primarily by synthetic smooth muscle cells, increases during atherogenesis. NG2 ablation unexpectedly results in decreased (30%) plaque development, despite aggravated obesity and hyperlipidemia. Mechanistic studies reveal that NG2-positive plaque synthetic smooth muscle cells in culture can sequester low-density lipoprotein to enhance foam-cell formation, processes in which NG2 itself plays direct roles. In agreement with these observations, low-density lipoprotein retention and lipid accumulation in the NG2/ApoE knockout aorta is 30% less than that seen in the control aorta.
    Conclusions: These results indicate that synthetic smooth muscle cell-dependent low-density lipoprotein retention and foam cell formation outweigh obesity and hyperlipidemia in promoting mouse atherogenesis. Our study sheds new light on the role of synthetic smooth muscle cells during atherogenesis. Blocking plaque NG2 or altering synthetic smooth muscle cells function may be promising therapeutic strategies for atherosclerosis.
    Mesh-Begriff(e) Animals ; Antigens/genetics ; Aorta/metabolism ; Aorta/pathology ; Aortic Diseases/genetics ; Aortic Diseases/metabolism ; Aortic Diseases/pathology ; Aortic Diseases/prevention & control ; Apolipoproteins E/deficiency ; Apolipoproteins E/genetics ; Atherosclerosis/genetics ; Atherosclerosis/metabolism ; Atherosclerosis/pathology ; Atherosclerosis/prevention & control ; Cells, Cultured ; Diet, High-Fat ; Disease Models, Animal ; Female ; Foam Cells/metabolism ; Foam Cells/pathology ; Hyperlipidemias/genetics ; Hyperlipidemias/metabolism ; Lipoproteins, LDL/metabolism ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle, Smooth, Vascular/metabolism ; Muscle, Smooth, Vascular/pathology ; Myocytes, Smooth Muscle/metabolism ; Myocytes, Smooth Muscle/pathology ; Obesity/genetics ; Obesity/metabolism ; Plaque, Atherosclerotic ; Proteoglycans/deficiency ; Proteoglycans/genetics
    Chemische Substanzen Antigens ; Apolipoproteins E ; Lipoproteins, LDL ; Proteoglycans ; chondroitin sulfate proteoglycan 4
    Sprache Englisch
    Erscheinungsdatum 2016-01
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1221433-4
    ISSN 1524-4636 ; 1079-5642
    ISSN (online) 1524-4636
    ISSN 1079-5642
    DOI 10.1161/ATVBAHA.115.306074
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Pleiotrophin, a multifunctional tumor promoter through induction of tumor angiogenesis, remodeling of the tumor microenvironment, and activation of stromal fibroblasts.

    Perez-Pinera, Pablo / Chang, Yunchao / Deuel, Thomas F

    Cell cycle (Georgetown, Tex.)

    2007  Band 6, Heft 23, Seite(n) 2877–2883

    Abstract: Pleiotrophin (PTN, Ptn) is a widely expressed, developmentally regulated 136 amino acid secreted heparin-binding cytokine. It signals through a unique signaling pathway; the PTN receptor is the transmembrane receptor protein tyrosine phosphatase (RPTP) ... ...

    Abstract Pleiotrophin (PTN, Ptn) is a widely expressed, developmentally regulated 136 amino acid secreted heparin-binding cytokine. It signals through a unique signaling pathway; the PTN receptor is the transmembrane receptor protein tyrosine phosphatase (RPTP)beta/zeta. RPTPbeta/zeta is inactivated by PTN, which leads to increased tyrosine phosphorylation of the downstream targets of the PTN/RPTPbeta/zeta signaling pathway. Pleiotrophin gene expression is found in cells in early differentiation during different developmental periods. It is upregulated in cells with an early differentiation phenotype in wound repair. The Ptn gene also is a proto-oncogene; PTN is expressed in human tumor cells, and, in cell lines derived from human tumors that express Ptn, Ptn expression is constitutive and thus "inappropriate". Importantly, properties of different cells induced by PTN in PTN-stimulated cells are strikingly similar to properties of highly malignant cells. Furthermore, transformed cells into which Ptn is introduced undergo "switches" to malignant cells of higher malignancy with properties that are strikingly similar to properties of PTN-stimulated cells. These unique features of PTN support the conclusion that constitutive PTN signaling in malignant cells that inappropriately express Ptn functions as a potent tumor promoter. Recently, in confirmation, Ptn targeted by the mouse mammary tumor virus (MMTV) promoter in a transgenic mouse model was found to promote breast cancers to a more aggressive breast cancer cell phenotype that morphologically closely resembles scirrhous carcinoma in human; in addition, it promoted a striking increase in tumor angiogenesis and a remarkable degree of remodeling of the micro-environment. Pleiotrophin thus regulates both different normal and pathological functions; collectively, the different studies have uncovered the unique ability of a single cytokine PTN, which signals through the unique PTN/RPTPbeta/zeta signaling pathway, to induce the many properties associated with tumor promotion in the malignant cells that constitutively express Ptn and in their microenvironment.
    Mesh-Begriff(e) Carrier Proteins/physiology ; Cytokines/physiology ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Growth Substances/physiology ; Humans ; Neoplasms/pathology ; Neovascularization, Pathologic/pathology ; Signal Transduction ; Stromal Cells/metabolism ; Stromal Cells/pathology
    Chemische Substanzen Carrier Proteins ; Cytokines ; Growth Substances ; pleiotrophin (134034-50-7)
    Sprache Englisch
    Erscheinungsdatum 2007-12-21
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.4161/cc.6.23.5090
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: Reduced inflammation accompanies diminished myelin damage and repair in the NG2 null mouse spinal cord.

    Kucharova, Karolina / Chang, Yunchao / Boor, Andrej / Yong, Voon Wee / Stallcup, William B

    Journal of neuroinflammation

    2011  Band 8, Seite(n) 158

    Abstract: Background: Multiple sclerosis (MS) is a demyelinating disease in which blood-derived immune cells and activated microglia damage myelin in the central nervous system. While oligodendrocyte progenitor cells (OPCs) are essential for generating ... ...

    Abstract Background: Multiple sclerosis (MS) is a demyelinating disease in which blood-derived immune cells and activated microglia damage myelin in the central nervous system. While oligodendrocyte progenitor cells (OPCs) are essential for generating oligodendrocytes for myelin repair, other cell types also participate in the damage and repair processes. The NG2 proteoglycan is expressed by OPCs, pericytes, and macrophages/microglia. In this report we investigate the effects of NG2 on these cell types during spinal cord demyelination/remyelination.
    Methods: Demyelinated lesions were created by microinjecting 1% lysolecithin into the lumbar spinal cord. Following demyelination, NG2 expression patterns in wild type mice were studied via immunostaining. Immunolabeling was also used in wild type and NG2 null mice to compare the extent of myelin damage, the kinetics of myelin repair, and the respective responses of OPCs, pericytes, and macrophages/microglia. Cell proliferation was quantified by studies of BrdU incorporation, and cytokine expression levels were evaluated using qRT-PCR.
    Results: The initial volume of spinal cord demyelination in wild type mice is twice as large as in NG2 null mice. However, over the ensuing 5 weeks there is a 6-fold improvement in myelination in wild type mice, versus only a 2-fold improvement in NG2 null mice. NG2 ablation also results in reduced numbers of each of the three affected cell types. BrdU incorporation studies reveal that reduced cell proliferation is an important factor underlying NG2-dependent decreases in each of the three key cell populations. In addition, NG2 ablation reduces macrophage/microglial cell migration and shifts cytokine expression from a pro-inflammatory to anti-inflammatory phenotype.
    Conclusions: Loss of NG2 expression leads to decreased proliferation of OPCs, pericytes, and macrophages/microglia, reducing the abundance of all three cell types in demyelinated spinal cord lesions. As a result of these NG2-dependent changes, the course of demyelination and remyelination in NG2 null mice differs from that seen in wild type mice, with both myelin damage and repair being reduced in the NG2 null mouse. These studies identify NG2 as an important factor in regulating myelin processing, suggesting that therapeutic targeting of the proteoglycan might offer a means of manipulating cell behavior in demyelinating diseases.
    Mesh-Begriff(e) Animals ; Antigens/genetics ; Antigens/metabolism ; Calcium-Binding Proteins/metabolism ; Cell Movement ; Cell Proliferation ; Cytokines/immunology ; Inflammation/immunology ; Inflammation/pathology ; Lysophosphatidylcholines/pharmacology ; Macrophages/cytology ; Macrophages/metabolism ; Mice ; Mice, Knockout ; Microfilament Proteins/metabolism ; Microglia/cytology ; Microglia/metabolism ; Multiple Sclerosis/immunology ; Multiple Sclerosis/pathology ; Myelin Sheath/drug effects ; Myelin Sheath/immunology ; Myelin Sheath/pathology ; Proteoglycans/genetics ; Proteoglycans/metabolism ; Receptor, Platelet-Derived Growth Factor alpha/metabolism ; Receptor, Platelet-Derived Growth Factor beta/metabolism ; Regeneration/physiology ; Spinal Cord/drug effects ; Spinal Cord/immunology ; Spinal Cord/pathology
    Chemische Substanzen Aif1 protein, mouse ; Antigens ; Calcium-Binding Proteins ; Cytokines ; Lysophosphatidylcholines ; Microfilament Proteins ; Proteoglycans ; chondroitin sulfate proteoglycan 4 ; Receptor, Platelet-Derived Growth Factor alpha (EC 2.7.10.1) ; Receptor, Platelet-Derived Growth Factor beta (EC 2.7.10.1)
    Sprache Englisch
    Erscheinungsdatum 2011-11-13
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 1742-2094
    ISSN (online) 1742-2094
    DOI 10.1186/1742-2094-8-158
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel ; Online: Disrupting the CH1 domain structure in the acetyltransferases CBP and p300 results in lean mice with increased metabolic control.

    Bedford, David C / Kasper, Lawryn H / Wang, Ruoning / Chang, Yunchao / Green, Douglas R / Brindle, Paul K

    Cell metabolism

    2011  Band 14, Heft 2, Seite(n) 219–230

    Abstract: Opposing activities of acetyltransferases and deacetylases help regulate energy balance. Mice heterozygous for the acetyltransferase CREB binding protein (CBP) are lean and insulin sensitized, but how CBP regulates energy homeostasis is unclear. In one ... ...

    Abstract Opposing activities of acetyltransferases and deacetylases help regulate energy balance. Mice heterozygous for the acetyltransferase CREB binding protein (CBP) are lean and insulin sensitized, but how CBP regulates energy homeostasis is unclear. In one model, the main CBP interaction with the glucagon-responsive factor CREB is not limiting for liver gluconeogenesis, whereas a second model posits that Ser436 in the CH1 (TAZ1) domain of CBP is required for insulin and the antidiabetic drug metformin to inhibit CREB-mediated liver gluconeogenesis. Here we show that conditional knockout of CBP in liver does not decrease fasting blood glucose or gluconeogenic gene expression, consistent with the first model. However, mice in which the CBP CH1 domain structure is disrupted by deleting residues 342-393 (ΔCH1) are lean and insulin sensitized, as are p300ΔCH1 mutants. CBP(ΔCH1/ΔCH1) mice remain metformin responsive. An intact CH1 domain is thus necessary for normal energy storage, but not for the blood glucose-lowering actions of insulin and metformin.
    Mesh-Begriff(e) Animals ; Blood Glucose/genetics ; CREB-Binding Protein/genetics ; CREB-Binding Protein/metabolism ; Cells, Cultured ; Diet ; Energy Metabolism ; Female ; Gluconeogenesis/genetics ; Insulin/metabolism ; Male ; Metformin/metabolism ; Mice ; Mice, Knockout ; Thinness/enzymology ; Thinness/genetics ; p300-CBP Transcription Factors/genetics ; p300-CBP Transcription Factors/metabolism
    Chemische Substanzen Blood Glucose ; Insulin ; Metformin (9100L32L2N) ; CREB-Binding Protein (EC 2.3.1.48) ; Crebbp protein, mouse (EC 2.3.1.48) ; p300-CBP Transcription Factors (EC 2.3.1.48) ; p300-CBP-associated factor (EC 2.3.1.48)
    Sprache Englisch
    Erscheinungsdatum 2011-06-24
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2176834-1
    ISSN 1932-7420 ; 1550-4131
    ISSN (online) 1932-7420
    ISSN 1550-4131
    DOI 10.1016/j.cmet.2011.06.010
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel: Disrupting the CH1 Domain Structure in the Acetyltransferases CBP and p300 Results in Lean Mice with Increased Metabolic Control

    Bedford, David C / Kasper, Lawryn H / Wang, Ruoning / Chang, Yunchao / Green, Douglas R / Brindle, Paul K

    Cell metabolism. 2011 Aug. 3, v. 14, no. 2

    2011  

    Abstract: Opposing activities of acetyltransferases and deacetylases help regulate energy balance. Mice heterozygous for the acetyltransferase CREB binding protein (CBP) are lean and insulin sensitized, but how CBP regulates energy homeostasis is unclear. In one ... ...

    Abstract Opposing activities of acetyltransferases and deacetylases help regulate energy balance. Mice heterozygous for the acetyltransferase CREB binding protein (CBP) are lean and insulin sensitized, but how CBP regulates energy homeostasis is unclear. In one model, the main CBP interaction with the glucagon-responsive factor CREB is not limiting for liver gluconeogenesis, whereas a second model posits that Ser436 in the CH1 (TAZ1) domain of CBP is required for insulin and the antidiabetic drug metformin to inhibit CREB-mediated liver gluconeogenesis. Here we show that conditional knockout of CBP in liver does not decrease fasting blood glucose or gluconeogenic gene expression, consistent with the first model. However, mice in which the CBP CH1 domain structure is disrupted by deleting residues 342–393 (ΔCH1) are lean and insulin sensitized, as are p300ΔCH1 mutants. CBPΔCH1/ΔCH1 mice remain metformin responsive. An intact CH1 domain is thus necessary for normal energy storage, but not for the blood glucose-lowering actions of insulin and metformin.
    Schlagwörter acetyltransferases ; binding proteins ; blood ; blood glucose ; energy balance ; fasting ; gene expression ; gluconeogenesis ; heterozygosity ; homeostasis ; insulin ; liver ; metformin ; mice ; models ; mutants
    Sprache Englisch
    Erscheinungsverlauf 2011-0803
    Umfang p. 219-230.
    Erscheinungsort Elsevier Inc.
    Dokumenttyp Artikel
    ZDB-ID 2176834-1
    ISSN 1932-7420 ; 1550-4131
    ISSN (online) 1932-7420
    ISSN 1550-4131
    DOI 10.1016/j.cmet.2011.06.010
    Datenquelle NAL Katalog (AGRICOLA)

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