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  1. Article: Mitochondrial autophagy: Origins, significance, and role of BNIP3 and NIX.

    Ney, Paul A

    Biochimica et biophysica acta

    2015  Volume 1853, Issue 10 Pt B, Page(s) 2775–2783

    Abstract: Mitochondrial autophagy (mitophagy) is a core cellular activity. In this review, we consider mitophagy and related cellular processes and discuss their significance for human disease. Strong parallels exist between mitophagy and xenophagy employed in ... ...

    Abstract Mitochondrial autophagy (mitophagy) is a core cellular activity. In this review, we consider mitophagy and related cellular processes and discuss their significance for human disease. Strong parallels exist between mitophagy and xenophagy employed in host defense. These mechanisms converge on receptors in the innate immune system in clinically relevant scenarios. Mitophagy is part of a cellular quality control mechanism, which is implicated in degenerative disease, especially neurodegenerative disease. Furthermore, mitophagy is an aspect of cellular remodeling, which is employed during development. BNIP3 and NIX are related multi-functional outer mitochondrial membrane proteins. BNIP3 regulates mitophagy during hypoxia, whereas NIX is required for mitophagy during development of the erythroid lineage. Recent advances in the field of BNIP3- and NIX-mediated mitophagy are discussed.
    MeSH term(s) Animals ; Autophagy/physiology ; Cell Hypoxia/physiology ; Erythroid Cells/cytology ; Erythroid Cells/metabolism ; Humans ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitochondrial Degradation/physiology ; Mitochondrial Membranes/metabolism ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism
    Chemical Substances BNIP3 protein, human ; BNIP3L protein, human ; Membrane Proteins ; Proto-Oncogene Proteins ; Tumor Suppressor Proteins
    Language English
    Publishing date 2015-10
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 60-7
    ISSN 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    ISSN (online) 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
    ISSN 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    DOI 10.1016/j.bbamcr.2015.02.022
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Another path to ERK activation.

    Ney, Paul A

    Blood

    2013  Volume 121, Issue 16, Page(s) 3064–3065

    MeSH term(s) Antigens, CD34/metabolism ; Cell Cycle Proteins/metabolism ; DNA-Binding Proteins/metabolism ; Erythroid Cells/cytology ; Erythropoiesis ; Erythropoietin/metabolism ; Humans ; MAP Kinase Signaling System ; Oncogene Proteins/metabolism ; raf Kinases/metabolism
    Chemical Substances Antigens, CD34 ; Cell Cycle Proteins ; DNA-Binding Proteins ; MFHAS1 protein, human ; Oncogene Proteins ; Erythropoietin (11096-26-7) ; raf Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2013-04-17
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2013-02-480459
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: c-Maf rules the island.

    Ney, Paul A

    Blood

    2011  Volume 118, Issue 5, Page(s) 1192–1193

    Language English
    Publishing date 2011-08-03
    Publishing country United States
    Document type Comment ; Journal Article
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2011-06-359752
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: The antileukemic activity of Δ12-PGJ3.

    Ney, Paul A

    Blood

    2011  Volume 118, Issue 26, Page(s) 6728–6729

    MeSH term(s) Animals ; Apoptosis/drug effects ; Fatty Acids, Omega-3/pharmacology ; Leukemia/drug therapy ; Neoplastic Stem Cells/drug effects ; Prostaglandins/pharmacology
    Chemical Substances Fatty Acids, Omega-3 ; Prostaglandins ; delta12-prostaglandin J3
    Language English
    Publishing date 2011-12-20
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2011-10-385328
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Normal and disordered reticulocyte maturation.

    Ney, Paul A

    Current opinion in hematology

    2011  Volume 18, Issue 3, Page(s) 152–157

    Abstract: Purpose of review: Reticulocyte remodeling has emerged as an important model for the understanding of vesicular trafficking and selective autophagy in mammalian cells. This review covers recent advances in our understanding of these processes in ... ...

    Abstract Purpose of review: Reticulocyte remodeling has emerged as an important model for the understanding of vesicular trafficking and selective autophagy in mammalian cells. This review covers recent advances in our understanding of these processes in reticulocytes and the role of these processes in erythroid development.
    Recent findings: Enucleation is caused by the coalescence of vesicles at the nuclear-cytoplasmic junction and microfilament contraction. Mitochondrial elimination is achieved through selective autophagy, in which mitochondria are targeted to autophagosomes, and undergo subsequent degradation and exocytosis. The mechanism involves an integral mitochondrial outer membrane protein and general autophagy pathways. Plasma membrane remodeling, and the elimination of certain intracellular organelles occur through the exosomal pathway.
    Summary: Vesicular trafficking and selective autophagy have emerged as central processes in cellular remodeling. In reticulocytes, this includes enucleation and the elimination of all membrane-bound organelles and ribosomes. Ubiquitin-like conjugation pathways, which are required for autophagy in yeast, are not essential for mitochondrial clearance in reticulocytes. Thus, in higher eukaryotes, there appears to be redundancy between these pathways and other processes, such as vesicular nucleation. Future studies will address the relationship between autophagy and vesicular trafficking, and the significance of both for cellular remodeling.
    MeSH term(s) Animals ; Autophagy ; Erythropoiesis ; Humans ; Reticulocytes/cytology ; Reticulocytes/metabolism ; Reticulocytes/pathology
    Language English
    Publishing date 2011-03-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1153887-9
    ISSN 1531-7048 ; 1065-6251
    ISSN (online) 1531-7048
    ISSN 1065-6251
    DOI 10.1097/MOH.0b013e328345213e
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: The reason sickle reticulocytes expose PS.

    Discher, Dennis E / Ney, Paul A

    Blood

    2015  Volume 126, Issue 15, Page(s) 1737–1738

    Abstract: In this issue of Blood, Mankelow et al link phosphatidylserine (PS) exposure in sickle erythrocytes to a physiological event in reticulocyte maturation. This discovery has implications for efforts to prevent thrombosis in sickle cell disease (SCD). ...

    Abstract In this issue of Blood, Mankelow et al link phosphatidylserine (PS) exposure in sickle erythrocytes to a physiological event in reticulocyte maturation. This discovery has implications for efforts to prevent thrombosis in sickle cell disease (SCD).
    MeSH term(s) Anemia, Sickle Cell/blood ; Anemia, Sickle Cell/pathology ; Autophagy ; Erythrocytes/pathology ; Humans ; Phosphatidylserines/metabolism ; Reticulocytes/pathology
    Chemical Substances Phosphatidylserines
    Language English
    Publishing date 2015-10-07
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2015-08-665117
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Gene expression during terminal erythroid differentiation.

    Ney, Paul A

    Current opinion in hematology

    2006  Volume 13, Issue 4, Page(s) 203–208

    Abstract: Purpose of review: Expression profiling is a powerful technique to sample cell state. This review shows how expression profiling is being applied to the study of erythroid differentiation.: Recent findings: Expression-based studies of multipotential ... ...

    Abstract Purpose of review: Expression profiling is a powerful technique to sample cell state. This review shows how expression profiling is being applied to the study of erythroid differentiation.
    Recent findings: Expression-based studies of multipotential hematopoietic progenitor cells has shown that these cells express lineage-restricted genes from multiple lineages at low levels, and that they are in effect 'primed' to develop into all hematopoietic cell types. Expression profiling of oligopotent and committed progenitor cells has further shown that commitment to the erythroid lineage is associated with a progressive decline in the number of expressed genes. Lineage commitment is regulated by lineage-restricted transcription factors, and studies show that the erythroid transcription factor GATA1, in addition to activating a subset of genes, has global repressive effects on gene expression. Terminal erythroid differentiation is associated with further reduction in the number of expressed genes. The erythroid program is defined by those genes that are still expressed, and their high-level expression depends on specific epigenetic modifications, recruitment of transcription factors, and posttranscriptional effects.
    Summary: Expression profiling provides the means to identify novel targets for the therapy of erythrocytes disorders, and to obtain insights into the mechanisms of cellular differentiation.
    MeSH term(s) Animals ; Cell Differentiation/genetics ; Erythropoiesis/genetics ; Gene Expression Profiling/trends ; Gene Expression Regulation/genetics ; Hematologic Diseases/genetics ; Hematologic Diseases/metabolism ; Humans ; Oligonucleotide Array Sequence Analysis
    Language English
    Publishing date 2006-07
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1153887-9
    ISSN 1531-7048 ; 1065-6251
    ISSN (online) 1531-7048
    ISSN 1065-6251
    DOI 10.1097/01.moh.0000231415.18333.2c
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Mechanisms and biology of B-cell leukemia/lymphoma 2/adenovirus E1B interacting protein 3 and Nip-like protein X.

    Zhang, Ji / Ney, Paul A

    Antioxidants & redox signaling

    2011  Volume 14, Issue 10, Page(s) 1959–1969

    Abstract: B-cell leukemia/lymphoma 2 (BCL-2)/adenovirus E1B interacting protein 3 (BNIP3) and Nip-like protein X (NIX) are atypical BCL-2 homology domain 3-only proteins involved in cell death, autophagy, and programmed mitochondrial clearance. BNIP3 and NIX cause ...

    Abstract B-cell leukemia/lymphoma 2 (BCL-2)/adenovirus E1B interacting protein 3 (BNIP3) and Nip-like protein X (NIX) are atypical BCL-2 homology domain 3-only proteins involved in cell death, autophagy, and programmed mitochondrial clearance. BNIP3 and NIX cause cell death by targeting mitochondria, directly through BCL-2-associated X protein- or BCL-2-antagonist/killer-dependent mechanisms, or indirectly through an effect on calcium stores in the endoplasmic reticulum. BNIP3 and NIX also induce autophagy through an effect on mitochondrial reactive oxygen species production, or by releasing Beclin 1 from inhibitory interactions with antiapoptotic BCL-2 family proteins. BNIP3 downregulates mitochondrial mass in hypoxic cells, whereas NIX is required for mitochondrial elimination during erythroid development. BNIP3 and NIX have an emerging role in human health. Cell death mediated by BNIP3 and NIX is implicated in heart disease and ischemic injury. Cancer progression is linked to loss of the prodeath function of BNIP3, but also to induction of its prosurvival activity. Finally, BNIP3 and NIX are implicated in mitochondrial quality control, which is important in aging and degenerative disease. Elucidation of the mechanisms by which BNIP3 and NIX regulate cell death, autophagy, and mitochondrial clearance may lead to treatments for these conditions.
    MeSH term(s) Animals ; Autophagy/physiology ; Humans ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitochondrial Proteins/genetics ; Mitochondrial Proteins/metabolism ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism ; bcl-2-Associated X Protein/genetics ; bcl-2-Associated X Protein/metabolism
    Chemical Substances BNIP3 protein, human ; BNIP3L protein, human ; BNip3 protein, mouse ; Membrane Proteins ; Mitochondrial Proteins ; Nix protein, mouse ; Proto-Oncogene Proteins ; Tumor Suppressor Proteins ; bcl-2-Associated X Protein
    Language English
    Publishing date 2011-03-04
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1483836-9
    ISSN 1557-7716 ; 1523-0864
    ISSN (online) 1557-7716
    ISSN 1523-0864
    DOI 10.1089/ars.2010.3772
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Reticulocyte mitophagy: monitoring mitochondrial clearance in a mammalian model.

    Zhang, Ji / Ney, Paul A

    Autophagy

    2010  Volume 6, Issue 3, Page(s) 405–408

    Abstract: Mitochondria are the primary site of energy production in animal cells. In mitochondria, the flow of electrons through the electron transport chain creates a potential difference across the inner membrane, which is utilized for ATP production. However, ... ...

    Abstract Mitochondria are the primary site of energy production in animal cells. In mitochondria, the flow of electrons through the electron transport chain creates a potential difference across the inner membrane, which is utilized for ATP production. However, due to inherent inefficiencies in electron transport, reactive oxygen species are also produced, which damage mitochondrial proteins and nucleic acids, and impair mitochondrial function. Decreased mitochondrial function causes increased reactive oxygen species generation, a decline in cellular function, and potentially cell death. Therefore, to maintain cellular homeostasis, mechanisms have evolved to selectively eliminate defective mitochondria. Mitochondria are constantly undergoing cycles of fission and fusion, and this process appears to have a role in mitochondrial quality control. Following fission, daughter mitochondria are produced, which can differ in their membrane polarization. Depolarized mitochondria are less likely to undergo subsequent fusion, and more likely to undergo autophagic clearance. As would be predicted, given the potential for cytochrome c release, depolarization is a powerful stimulus for mitochondrial clearance. Depolarization causes recruitment of the E3 ubiquitin ligase Parkin to mitochondria, which is required for their subsequent engulfment by autophagosomes. Macroautophagy pathways also appear to have a role, as hepatocytes deficient for the E1-like enzyme Atg7 accumulate abnormal mitochondria. Finally, recent studies in a developmental model have yielded insight into this process. Newly formed erythrocytes, also known as reticulocytes, eliminate their entire cohort of mitochondria during development. This process depends on the mitochondrial protein NIX, is partially dependent on autophagy, and is independent of mitochondrial depolarization. Here we describe the use of reticulocytes to study mitochondrial clearance.
    MeSH term(s) Animals ; Autophagy/physiology ; Cells, Cultured ; Flow Cytometry/methods ; Mice ; Mitochondria/metabolism ; Reticulocytes/cytology
    Language English
    Publishing date 2010-04-18
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.4161/auto.6.3.11245
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Requirement for antiapoptotic MCL-1 during early erythropoiesis.

    Turnis, Meghan E / Kaminska, Ewa / Smith, Kaitlyn H / Kartchner, Brittany J / Vogel, Peter / Laxton, Jonathan D / Ashmun, Richard A / Ney, Paul A / Opferman, Joseph T

    Blood

    2021  Volume 137, Issue 14, Page(s) 1945–1958

    Abstract: Although BCL-xL is critical to the survival of mature erythrocytes, it is still unclear whether other antiapoptotic molecules mediate survival during earlier stages of erythropoiesis. Here, we demonstrate that erythroid-specific Mcl1 deletion results in ... ...

    Abstract Although BCL-xL is critical to the survival of mature erythrocytes, it is still unclear whether other antiapoptotic molecules mediate survival during earlier stages of erythropoiesis. Here, we demonstrate that erythroid-specific Mcl1 deletion results in embryonic lethality beyond embryonic day 13.5 as a result of severe anemia caused by a lack of mature red blood cells (RBCs). Mcl1-deleted embryos exhibit stunted growth, ischemic necrosis, and decreased RBCs in the blood. Furthermore, we demonstrate that MCL-1 is only required during early definitive erythropoiesis; during later stages, developing erythrocytes become MCL-1 independent and upregulate the expression of BCL-xL. Functionally, MCL-1 relies upon its ability to prevent apoptosis to promote erythroid development because codeletion of the proapoptotic effectors Bax and Bak can overcome the requirement for MCL-1 expression. Furthermore, ectopic expression of human BCL2 in erythroid progenitors can compensate for Mcl1 deletion, indicating redundancy between these 2 antiapoptotic family members. These data clearly demonstrate a requirement for MCL-1 in promoting survival of early erythroid progenitors.
    MeSH term(s) Anemia/genetics ; Anemia/pathology ; Animals ; Apoptosis ; Cells, Cultured ; Embryo Loss/genetics ; Embryo Loss/pathology ; Erythrocytes/pathology ; Erythroid Cells/pathology ; Erythropoiesis ; Gene Deletion ; Gene Expression Regulation, Developmental ; Humans ; Mice, Inbred C57BL ; Myeloid Cell Leukemia Sequence 1 Protein/genetics ; Mice
    Chemical Substances Mcl1 protein, mouse ; Myeloid Cell Leukemia Sequence 1 Protein
    Language English
    Publishing date 2021-01-28
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2020006916
    Database MEDical Literature Analysis and Retrieval System OnLINE

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