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  1. AU="Xue, Jumin"
  2. AU="Nampota, Nginache"
  3. AU="de Carvalho, Vinicius S"
  4. AU=Eisen Michael B
  5. AU="Manal S. Selim" AU="Manal S. Selim"
  6. AU="Alturki, Ramadan"
  7. AU="Kluger, Benzi"
  8. AU="Mitchell, Krista"
  9. AU="Oakes, Mary"
  10. AU="Kevill, Dennis N"
  11. AU="Rojas, Almudena"
  12. AU=Dalmau Josep AU=Dalmau Josep
  13. AU="Vaňáčová, Štěpánka"
  14. AU="Hancioglu, Baris"
  15. AU="Scribner, Kim T"
  16. AU="Emanuel Schmassmann"
  17. AU="Patel, Monica"
  18. AU=Passariello Margherita
  19. AU=Saikia Bedangshu
  20. AU="Dion, Dominique"
  21. AU="Magami, Shunsuke"
  22. AU="Wagner, Henrik"

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  1. Artikel ; Online: Key transcriptional effectors of the pancreatic acinar phenotype and oncogenic transformation.

    Azevedo-Pouly, Ana / Hale, Michael A / Swift, Galvin H / Hoang, Chinh Q / Deering, Tye G / Xue, Jumin / Wilkie, Thomas M / Murtaugh, L Charles / MacDonald, Raymond J

    PloS one

    2023  Band 18, Heft 10, Seite(n) e0291512

    Abstract: Proper maintenance of mature cellular phenotypes is essential for stable physiology, suppression of disease states, and resistance to oncogenic transformation. We describe the transcriptional regulatory roles of four key DNA-binding transcription factors ...

    Abstract Proper maintenance of mature cellular phenotypes is essential for stable physiology, suppression of disease states, and resistance to oncogenic transformation. We describe the transcriptional regulatory roles of four key DNA-binding transcription factors (Ptf1a, Nr5a2, Foxa2 and Gata4) that sit at the top of a regulatory hierarchy controlling all aspects of a highly differentiated cell-type-the mature pancreatic acinar cell (PAC). Selective inactivation of Ptf1a, Nr5a2, Foxa2 and Gata4 individually in mouse adult PACs rapidly altered the transcriptome and differentiation status of PACs. The changes most emphatically included transcription of the genes for the secretory digestive enzymes (which conscript more than 90% of acinar cell protein synthesis), a potent anabolic metabolism that provides the energy and materials for protein synthesis, suppressed and properly balanced cellular replication, and susceptibility to transformation by oncogenic KrasG12D. The simultaneous inactivation of Foxa2 and Gata4 caused a greater-than-additive disruption of gene expression and uncovered their collaboration to maintain Ptf1a expression and control PAC replication. A measure of PAC dedifferentiation ranked the effects of the conditional knockouts as Foxa2+Gata4 > Ptf1a > Nr5a2 > Foxa2 > Gata4. Whereas the loss of Ptf1a or Nr5a2 greatly accelerated Kras-mediated transformation of mature acinar cells in vivo, the absence of Foxa2, Gata4, or Foxa2+Gata4 together blocked transformation completely, despite extensive dedifferentiation. A lack of correlation between PAC dedifferentiation and sensitivity to oncogenic KrasG12D negates the simple proposition that the level of differentiation determines acinar cell resistance to transformation.
    Mesh-Begriff(e) Mice ; Animals ; Acinar Cells/metabolism ; Pancreas, Exocrine ; Epithelium/metabolism ; Transcription Factors/genetics ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Phenotype ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/metabolism
    Chemische Substanzen Transcription Factors
    Sprache Englisch
    Erscheinungsdatum 2023-10-05
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0291512
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Autophagy collaborates with apoptosis pathways to control oligodendrocyte number.

    Zhang, Tingxin / Bhambri, Aksheev / Zhang, Yihe / Barbosa, Daniela / Bae, Han-Gyu / Xue, Jumin / Wazir, Sabeen / Mulinyawe, Sara B / Kim, Jun Hee / Sun, Lu O

    Cell reports

    2023  Band 42, Heft 8, Seite(n) 112943

    Abstract: Oligodendrocytes are the sole myelin-producing cells in the central nervous system. Oligodendrocyte number is tightly controlled across diverse brain regions to match local axon type and number, yet the underlying mechanisms remain unclear. Here, we show ...

    Abstract Oligodendrocytes are the sole myelin-producing cells in the central nervous system. Oligodendrocyte number is tightly controlled across diverse brain regions to match local axon type and number, yet the underlying mechanisms remain unclear. Here, we show that autophagy, an evolutionarily conserved cellular process that promotes cell survival under physiological conditions, elicits premyelinating oligodendrocyte apoptosis during development. Autophagy flux is increased in premyelinating oligodendrocytes, and its genetic blockage causes ectopic oligodendrocyte survival throughout the entire brain. Autophagy functions cell autonomously in the premyelinating oligodendrocyte to trigger cell apoptosis, and it genetically interacts with the TFEB pathway to limit oligodendrocyte number across diverse brain regions. Our results provide in vivo evidence showing that autophagy promotes apoptosis in mammalian cells under physiological conditions and reveal key intrinsic mechanisms governing oligodendrogenesis.
    Mesh-Begriff(e) Animals ; Oligodendroglia/metabolism ; Myelin Sheath/metabolism ; Axons ; Apoptosis ; Autophagy ; Cell Differentiation/physiology ; Mammals
    Sprache Englisch
    Erscheinungsdatum 2023-08-06
    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.
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2023.112943
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel: Autophagy collaborates with apoptosis pathways to control myelination specificity and function.

    Zhang, Tingxin / Bae, Han-Gyu / Bhambri, Aksheev / Zhang, Yihe / Barbosa, Daniela / Xue, Jumin / Wazir, Sabeen / Mulinyawe, Sara B / Kim, Jun Hee / Sun, Lu O

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Oligodendrocytes are the sole myelin producing cells in the central nervous system. Oligodendrocyte numbers are tightly controlled across diverse brain regions to match local axon type and number, but the underlying mechanisms and functional significance ...

    Abstract Oligodendrocytes are the sole myelin producing cells in the central nervous system. Oligodendrocyte numbers are tightly controlled across diverse brain regions to match local axon type and number, but the underlying mechanisms and functional significance remain unclear. Here, we show that autophagy, an evolutionarily conserved cellular process that promotes cell survival under canonical settings, elicits premyelinating oligodendrocyte apoptosis during development and regulates critical aspects of nerve pulse propagation. Autophagy flux is increased in premyelinating oligodendrocytes, and its genetic blockage causes ectopic oligodendrocyte survival throughout the entire brain. Autophagy acts in the TFEB-Bax/Bak pathway and elevates
    Highlights: Autophagy flux increases in the premyelinating and myelinating oligodendrocytesAutophagy promotes premyelinating oligodendrocyte (pre-OL) apoptosis to control myelination location and timing Autophagy acts in the TFEB-PUMA-Bax/Bak pathway and elevates
    Sprache Englisch
    Erscheinungsdatum 2023-01-02
    Erscheinungsland United States
    Dokumenttyp Preprint
    DOI 10.1101/2022.12.31.522394
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: The nuclear hormone receptor family member NR5A2 controls aspects of multipotent progenitor cell formation and acinar differentiation during pancreatic organogenesis.

    Hale, Michael A / Swift, Galvin H / Hoang, Chinh Q / Deering, Tye G / Masui, Toshi / Lee, Youn-Kyoung / Xue, Jumin / MacDonald, Raymond J

    Development (Cambridge, England)

    2014  Band 141, Heft 16, Seite(n) 3123–3133

    Abstract: The orphan nuclear receptor NR5A2 is necessary for the stem-like properties of the epiblast of the pre-gastrulation embryo and for cellular and physiological homeostasis of endoderm-derived organs postnatally. Using conditional gene inactivation, we show ...

    Abstract The orphan nuclear receptor NR5A2 is necessary for the stem-like properties of the epiblast of the pre-gastrulation embryo and for cellular and physiological homeostasis of endoderm-derived organs postnatally. Using conditional gene inactivation, we show that Nr5a2 also plays crucial regulatory roles during organogenesis. During the formation of the pancreas, Nr5a2 is necessary for the expansion of the nascent pancreatic epithelium, for the subsequent formation of the multipotent progenitor cell (MPC) population that gives rise to pre-acinar cells and bipotent cells with ductal and islet endocrine potential, and for the formation and differentiation of acinar cells. At birth, the NR5A2-deficient pancreas has defects in all three epithelial tissues: a partial loss of endocrine cells, a disrupted ductal tree and a >90% deficit of acini. The acinar defects are due to a combination of fewer MPCs, deficient allocation of those MPCs to pre-acinar fate, disruption of acinar morphogenesis and incomplete acinar cell differentiation. NR5A2 controls these developmental processes directly as well as through regulatory interactions with other pancreatic transcriptional regulators, including PTF1A, MYC, GATA4, FOXA2, RBPJL and MIST1 (BHLHA15). In particular, Nr5a2 and Ptf1a establish mutually reinforcing regulatory interactions and collaborate to control developmentally regulated pancreatic genes by binding to shared transcriptional regulatory regions. At the final stage of acinar cell development, the absence of NR5A2 affects the expression of Ptf1a and its acinar specific partner Rbpjl, so that the few acinar cells that form do not complete differentiation. Nr5a2 controls several temporally distinct stages of pancreatic development that involve regulatory mechanisms relevant to pancreatic oncogenesis and the maintenance of the exocrine phenotype.
    Mesh-Begriff(e) Acinar Cells/cytology ; Animals ; Base Sequence ; Cell Differentiation ; Cell Lineage ; Cell Proliferation ; Gene Expression Regulation, Developmental ; Male ; Mice ; Mice, Transgenic ; Mutation ; Pancreas/embryology ; Pancreas/growth & development ; Phenotype ; Receptors, Cytoplasmic and Nuclear/genetics ; Receptors, Cytoplasmic and Nuclear/physiology ; Stem Cells/cytology ; Transgenes
    Chemische Substanzen Nr5a2 protein, mouse ; Receptors, Cytoplasmic and Nuclear
    Sprache Englisch
    Erscheinungsdatum 2014-07-25
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 90607-4
    ISSN 1477-9129 ; 0950-1991
    ISSN (online) 1477-9129
    ISSN 0950-1991
    DOI 10.1242/dev.109405
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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