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  1. Article ; Online: A parathyroid hormone/salt-inducible kinase signaling axis controls renal vitamin D activation and organismal calcium homeostasis.

    Yoon, Sung-Hee / Meyer, Mark B / Arevalo, Carlos / Tekguc, Murat / Zhang, Chengcheng / Wang, Jialiang S / Castro Andrade, Christian D / Strauss, Katelyn / Sato, Tadatoshi / Benkusky, Nancy A / Lee, Seong Min / Berdeaux, Rebecca / Foretz, Marc / Sundberg, Thomas B / Xavier, Ramnik J / Adelmann, Charles H / Brooks, Daniel J / Anselmo, Anthony / Sadreyev, Ruslan I /
    Rosales, Ivy A / Fisher, David E / Gupta, Navin / Morizane, Ryuji / Greka, Anna / Pike, J Wesley / Mannstadt, Michael / Wein, Marc N

    The Journal of clinical investigation

    2023  Volume 133, Issue 9

    Abstract: The renal actions of parathyroid hormone (PTH) promote 1,25-vitamin D generation; however, the signaling mechanisms that control PTH-dependent vitamin D activation remain unknown. Here, we demonstrated that salt-inducible kinases (SIKs) orchestrated ... ...

    Abstract The renal actions of parathyroid hormone (PTH) promote 1,25-vitamin D generation; however, the signaling mechanisms that control PTH-dependent vitamin D activation remain unknown. Here, we demonstrated that salt-inducible kinases (SIKs) orchestrated renal 1,25-vitamin D production downstream of PTH signaling. PTH inhibited SIK cellular activity by cAMP-dependent PKA phosphorylation. Whole-tissue and single-cell transcriptomics demonstrated that both PTH and pharmacologic SIK inhibitors regulated a vitamin D gene module in the proximal tubule. SIK inhibitors increased 1,25-vitamin D production and renal Cyp27b1 mRNA expression in mice and in human embryonic stem cell-derived kidney organoids. Global- and kidney-specific Sik2/Sik3 mutant mice showed Cyp27b1 upregulation, elevated serum 1,25-vitamin D, and PTH-independent hypercalcemia. The SIK substrate CRTC2 showed PTH and SIK inhibitor-inducible binding to key Cyp27b1 regulatory enhancers in the kidney, which were also required for SIK inhibitors to increase Cyp27b1 in vivo. Finally, in a podocyte injury model of chronic kidney disease-mineral bone disorder (CKD-MBD), SIK inhibitor treatment stimulated renal Cyp27b1 expression and 1,25-vitamin D production. Together, these results demonstrated a PTH/SIK/CRTC signaling axis in the kidney that controls Cyp27b1 expression and 1,25-vitamin D synthesis. These findings indicate that SIK inhibitors might be helpful for stimulation of 1,25-vitamin D production in CKD-MBD.
    MeSH term(s) Mice ; Humans ; Animals ; Vitamin D/metabolism ; Parathyroid Hormone/genetics ; Parathyroid Hormone/metabolism ; Calcium/metabolism ; 25-Hydroxyvitamin D3 1-alpha-Hydroxylase/metabolism ; Chronic Kidney Disease-Mineral and Bone Disorder/metabolism ; Kidney/metabolism ; Renal Insufficiency, Chronic/metabolism ; Homeostasis ; Protein Serine-Threonine Kinases/genetics ; Protein Serine-Threonine Kinases/metabolism
    Chemical Substances Vitamin D (1406-16-2) ; Parathyroid Hormone ; Calcium (SY7Q814VUP) ; 25-Hydroxyvitamin D3 1-alpha-Hydroxylase (EC 1.14.15.18) ; SIK3 protein, mouse (EC 2.7.11.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2023-05-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI163627
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  2. Article ; Online: TREM2 Acts Downstream of CD33 in Modulating Microglial Pathology in Alzheimer's Disease.

    Griciuc, Ana / Patel, Shaun / Federico, Anthony N / Choi, Se Hoon / Innes, Brendan J / Oram, Mary K / Cereghetti, Gea / McGinty, Danielle / Anselmo, Anthony / Sadreyev, Ruslan I / Hickman, Suzanne E / El Khoury, Joseph / Colonna, Marco / Tanzi, Rudolph E

    Neuron

    2019  Volume 103, Issue 5, Page(s) 820–835.e7

    Abstract: The microglial receptors CD33 and TREM2 have been associated with risk for Alzheimer's disease (AD). Here, we investigated crosstalk between CD33 and TREM2. We showed that knockout of CD33 attenuated amyloid beta (Aβ) pathology and improved cognition in ... ...

    Abstract The microglial receptors CD33 and TREM2 have been associated with risk for Alzheimer's disease (AD). Here, we investigated crosstalk between CD33 and TREM2. We showed that knockout of CD33 attenuated amyloid beta (Aβ) pathology and improved cognition in 5xFAD mice, both of which were abrogated by additional TREM2 knockout. Knocking out TREM2 in 5xFAD mice exacerbated Aβ pathology and neurodegeneration but reduced Iba1
    MeSH term(s) Acute-Phase Reaction/genetics ; Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/metabolism ; Animals ; Brain/metabolism ; Brain/pathology ; Cognition ; Disease Models, Animal ; Gene Expression Regulation ; Interleukin-6/metabolism ; Interleukin-8/metabolism ; Membrane Glycoproteins/genetics ; Mice ; Mice, Knockout ; Microglia/metabolism ; Microglia/pathology ; Phagocytosis/genetics ; Plaque, Amyloid/pathology ; Receptors, Immunologic/genetics ; Sialic Acid Binding Ig-like Lectin 3/genetics
    Chemical Substances Amyloid beta-Peptides ; Cd33 protein, mouse ; Interleukin-6 ; Interleukin-8 ; Membrane Glycoproteins ; Receptors, Immunologic ; Sialic Acid Binding Ig-like Lectin 3 ; Trem2 protein, mouse ; interleukin-6, mouse
    Language English
    Publishing date 2019-07-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 808167-0
    ISSN 1097-4199 ; 0896-6273
    ISSN (online) 1097-4199
    ISSN 0896-6273
    DOI 10.1016/j.neuron.2019.06.010
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  3. Article ; Online: A parathyroid hormone/salt-inducible kinase signaling axis controls renal vitamin D activation and organismal calcium homeostasis

    Sung-Hee Yoon / Mark B. Meyer / Carlos Arevalo / Murat Tekguc / Chengcheng Zhang / Jialiang S. Wang / Christian D. Castro Andrade / Katelyn Strauss / Tadatoshi Sato / Nancy A. Benkusky / Seong Min Lee / Rebecca Berdeaux / Marc Foretz / Thomas B. Sundberg / Ramnik J. Xavier / Charles H. Adelmann / Daniel J. Brooks / Anthony Anselmo / Ruslan I. Sadreyev /
    Ivy A. Rosales / David E. Fisher / Navin Gupta / Ryuji Morizane / Anna Greka / J. Wesley Pike / Michael Mannstadt / Marc N. Wein

    The Journal of Clinical Investigation, Vol 133, Iss

    2023  Volume 9

    Abstract: The renal actions of parathyroid hormone (PTH) promote 1,25-vitamin D generation; however, the signaling mechanisms that control PTH-dependent vitamin D activation remain unknown. Here, we demonstrated that salt-inducible kinases (SIKs) orchestrated ... ...

    Abstract The renal actions of parathyroid hormone (PTH) promote 1,25-vitamin D generation; however, the signaling mechanisms that control PTH-dependent vitamin D activation remain unknown. Here, we demonstrated that salt-inducible kinases (SIKs) orchestrated renal 1,25-vitamin D production downstream of PTH signaling. PTH inhibited SIK cellular activity by cAMP-dependent PKA phosphorylation. Whole-tissue and single-cell transcriptomics demonstrated that both PTH and pharmacologic SIK inhibitors regulated a vitamin D gene module in the proximal tubule. SIK inhibitors increased 1,25-vitamin D production and renal Cyp27b1 mRNA expression in mice and in human embryonic stem cell–derived kidney organoids. Global- and kidney-specific Sik2/Sik3 mutant mice showed Cyp27b1 upregulation, elevated serum 1,25-vitamin D, and PTH-independent hypercalcemia. The SIK substrate CRTC2 showed PTH and SIK inhibitor–inducible binding to key Cyp27b1 regulatory enhancers in the kidney, which were also required for SIK inhibitors to increase Cyp27b1 in vivo. Finally, in a podocyte injury model of chronic kidney disease–mineral bone disorder (CKD-MBD), SIK inhibitor treatment stimulated renal Cyp27b1 expression and 1,25-vitamin D production. Together, these results demonstrated a PTH/SIK/CRTC signaling axis in the kidney that controls Cyp27b1 expression and 1,25-vitamin D synthesis. These findings indicate that SIK inhibitors might be helpful for stimulation of 1,25-vitamin D production in CKD-MBD.
    Keywords Bone Biology ; Nephrology ; Medicine ; R
    Subject code 616
    Language English
    Publishing date 2023-05-01T00:00:00Z
    Publisher American Society for Clinical Investigation
    Document type Article ; Online
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  4. Article ; Online: Protein kinase function and glutathionylation.

    Anselmo, Anthony N / Cobb, Melanie H

    The Biochemical journal

    2004  Volume 381, Issue Pt 3, Page(s) e1–2

    Abstract: Intracellular reactive oxygen species are generated as a by-product of normal metabolic processes and can both damage cellular constituents and function as important signalling species. This signalling often involves changes in the thiol redox balance. ... ...

    Abstract Intracellular reactive oxygen species are generated as a by-product of normal metabolic processes and can both damage cellular constituents and function as important signalling species. This signalling often involves changes in the thiol redox balance. As an antioxidant, glutathione serves in maintaining the reduced state of cellular protein thiol groups. The paper by Cross and Templeton appearing in this issue of the Biochemical Journal describes a mechanism by which glutathionylation plays a key role in the regulation of the kinase activity of MEKK1 [MAP (mitogen-activated protein kinase)/ERK (extracellular-signal-regulated kinase) kinase kinase; MAP3K] in response to oxidative stresses. This type of post-translational-modification glutathionylation may represent a general mechanism by which protein kinase function can be regulated.
    MeSH term(s) Glutathione/chemistry ; Protein Kinases/chemistry ; Protein Kinases/physiology
    Chemical Substances Protein Kinases (EC 2.7.-) ; Glutathione (GAN16C9B8O)
    Language English
    Publishing date 2004-07-21
    Publishing country England
    Document type Comment ; Journal Article ; Review
    ZDB-ID 2969-5
    ISSN 1470-8728 ; 0006-2936 ; 0306-3275 ; 0264-6021
    ISSN (online) 1470-8728
    ISSN 0006-2936 ; 0306-3275 ; 0264-6021
    DOI 10.1042/BJ20040873
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  5. Article ; Online: T Cell Immune Deficiency in

    Moore, John C / Mulligan, Timothy S / Yordán, Nora Torres / Castranova, Daniel / Pham, Van N / Tang, Qin / Lobbardi, Riadh / Anselmo, Anthony / Liwski, Robert S / Berman, Jason N / Sadreyev, Ruslan I / Weinstein, Brant M / Langenau, David M

    Molecular and cellular biology

    2016  Volume 36, Issue 23, Page(s) 2868–2876

    Abstract: ... ...

    Abstract ZAP70
    Language English
    Publishing date 2016-11-14
    Publishing country United States
    Document type Journal Article
    ZDB-ID 779397-2
    ISSN 1098-5549 ; 0270-7306
    ISSN (online) 1098-5549
    ISSN 0270-7306
    DOI 10.1128/MCB.00281-16
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  6. Article ; Online: Functional genomics reveals that tumors with activating phosphoinositide 3-kinase mutations are dependent on accelerated protein turnover.

    Davoli, Teresa / Mengwasser, Kristen E / Duan, Jingjing / Chen, Ting / Christensen, Camilla / Wooten, Eric C / Anselmo, Anthony N / Li, Mamie Z / Wong, Kwok-Kin / Kahle, Kristopher T / Elledge, Stephen J

    Genes & development

    2017  Volume 30, Issue 24, Page(s) 2684–2695

    Abstract: Activating mutations in the phosphoinositide 3-kinase (PI3K) signaling pathway are frequently identified in cancer. To identify pathways that support PI3K oncogenesis, we performed a genome-wide RNAi screen in isogenic cell lines harboring wild-type or ... ...

    Abstract Activating mutations in the phosphoinositide 3-kinase (PI3K) signaling pathway are frequently identified in cancer. To identify pathways that support PI3K oncogenesis, we performed a genome-wide RNAi screen in isogenic cell lines harboring wild-type or mutant PIK3CA to search for PI3K synthetic-lethal (SL) genes. A combined analysis of these results with a meta-analysis of two other large-scale RNAi screening data sets in PI3K mutant cancer cell lines converged on ribosomal protein translation and proteasomal protein degradation as critical nononcogene dependencies for PI3K-driven tumors. Genetic or pharmacologic inhibition of either pathway alone, but not together, selectively killed PI3K mutant tumor cells in an mTOR-dependent manner. The expression of ribosomal and proteasomal components was significantly up-regulated in primary human colorectal tumors harboring PI3K pathway activation. Importantly, a PI3K SL gene signature containing the top hits of the SL genes identified in our meta-analysis robustly predicted overall patient survival in colorectal cancer, especially among patients with tumors with an activated PI3K pathway. These results suggest that disruption of protein turnover homeostasis via ribosome or proteasome inhibition may be a novel treatment strategy for PI3K mutant human tumors.
    MeSH term(s) Animals ; Colorectal Neoplasms/diagnosis ; Colorectal Neoplasms/enzymology ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/physiopathology ; Gene Expression Regulation, Neoplastic ; Genomics ; HCT116 Cells ; HEK293 Cells ; Humans ; Mice ; Mutation ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Proteasome Endopeptidase Complex/genetics ; Ribosomes/genetics ; Signal Transduction/genetics
    Chemical Substances Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
    Keywords covid19
    Language English
    Publishing date 2017-01-10
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
    ZDB-ID 806684-x
    ISSN 1549-5477 ; 0890-9369
    ISSN (online) 1549-5477
    ISSN 0890-9369
    DOI 10.1101/gad.290122.116
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  7. Article ; Online: tiRNA signaling via stress-regulated vesicle transfer in the hematopoietic niche.

    Kfoury, Youmna S / Ji, Fei / Mazzola, Michael / Sykes, David B / Scherer, Allison K / Anselmo, Anthony / Akiyama, Yasutoshi / Mercier, Francois / Severe, Nicolas / Kokkaliaris, Konstantinos D / Zhao, Ting / Brouse, Thomas / Saez, Borja / Seidl, Jefferson / Papazian, Ani / Ivanov, Pavel / Mansour, Michael K / Sadreyev, Ruslan I / Scadden, David T

    Cell stem cell

    2021  Volume 28, Issue 12, Page(s) 2090–2103.e9

    Abstract: Extracellular vesicles (EVs) transfer complex biologic material between cells. However, the role of this process in vivo is poorly defined. Here, we demonstrate that osteoblastic cells in the bone marrow (BM) niche elaborate extracellular vesicles that ... ...

    Abstract Extracellular vesicles (EVs) transfer complex biologic material between cells. However, the role of this process in vivo is poorly defined. Here, we demonstrate that osteoblastic cells in the bone marrow (BM) niche elaborate extracellular vesicles that are taken up by hematopoietic progenitor cells in vivo. Genotoxic or infectious stress rapidly increased stromal-derived extracellular vesicle transfer to granulocyte-monocyte progenitors. The extracellular vesicles contained processed tRNAs (tiRNAs) known to modulate protein translation. 5'-ti-Pro-CGG-1 was preferentially abundant in osteoblast-derived extracellular vesicles and, when transferred to granulocyte-monocyte progenitors, increased protein translation, cell proliferation, and myeloid differentiation. Upregulating EV transfer improved hematopoietic recovery from genotoxic injury and survival from fungal sepsis. Therefore, EV-mediated tiRNA transfer provides a stress-modulated signaling axis in the BM niche distinct from conventional cytokine-driven stress responses.
    MeSH term(s) Bone Marrow ; Bone Marrow Cells ; Extracellular Vesicles ; Hematopoiesis ; Hematopoietic Stem Cells
    Language English
    Publishing date 2021-09-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2375354-7
    ISSN 1875-9777 ; 1934-5909
    ISSN (online) 1875-9777
    ISSN 1934-5909
    DOI 10.1016/j.stem.2021.08.014
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  8. Article: HELZ2 Is an IFN Effector Mediating Suppression of Dengue Virus.

    Fusco, Dahlene N / Pratt, Henry / Kandilas, Stephen / Cheon, Scarlett Se Yun / Lin, Wenyu / Cronkite, D Alex / Basavappa, Megha / Jeffrey, Kate L / Anselmo, Anthony / Sadreyev, Ruslan / Yapp, Clarence / Shi, Xu / O'Sullivan, John F / Gerszten, Robert E / Tomaru, Takuya / Yoshino, Satoshi / Satoh, Tetsurou / Chung, Raymond T

    Frontiers in microbiology

    2017  Volume 8, Page(s) 240

    Abstract: Flaviviral infections including dengue virus are an increasing clinical problem worldwide. Dengue infection triggers host production of the type 1 IFN, IFN alpha, one of the strongest and broadest acting antivirals known. However, dengue virus subverts ... ...

    Abstract Flaviviral infections including dengue virus are an increasing clinical problem worldwide. Dengue infection triggers host production of the type 1 IFN, IFN alpha, one of the strongest and broadest acting antivirals known. However, dengue virus subverts host IFN signaling at early steps of IFN signal transduction. This subversion allows unbridled viral replication which subsequently triggers ongoing production of IFN which, again, is subverted. Identification of downstream IFN antiviral effectors will provide targets which could be activated to restore broad acting antiviral activity, stopping the signal to produce endogenous IFN at toxic levels. To this end, we performed a targeted functional genomic screen for IFN antiviral effector genes (IEGs), identifying 56 IEGs required for antiviral effects of IFN against fully infectious dengue virus. Dengue IEGs were enriched for genes encoding nuclear receptor interacting proteins, including HELZ2, MAP2K4, SLC27A2, HSP90AA1, and HSP90AB1. We focused on HELZ2 (Helicase With Zinc Finger 2), an IFN stimulated gene and IEG which encodes a promiscuous nuclear factor coactivator that exists in two isoforms. The two unique HELZ2 isoforms are both IFN responsive, contain ISRE elements, and gene products increase in the nucleus upon IFN stimulation. Chromatin immunoprecipitation-sequencing revealed that the HELZ2 complex interacts with triglyceride-regulator LMF1. Mass spectrometry revealed that HELZ2 knockdown cells are depleted of triglyceride subsets. We thus sought to determine whether HELZ2 interacts with a nuclear receptor known to regulate immune response and lipid metabolism, AHR, and identified HELZ2:AHR interactions via co-immunoprecipitation, found that AHR is a dengue IEG, and that an AHR ligand, FICZ, exhibits anti-dengue activity. Primary bone marrow derived macrophages from HELZ2 knockout mice, compared to wild type controls, exhibit enhanced dengue infectivity. Overall, these findings reveal that IFN antiviral response is mediated by HELZ2 transcriptional upregulation, enrichment of HELZ2 protein levels in the nucleus, and activation of a transcriptional program that appears to modulate intracellular lipid state. IEGs identified in this study may serve as both (1) potential targets for host directed antiviral design, downstream of the common flaviviral subversion point, as well as (2) possible biomarkers, whose variation, natural, or iatrogenic, could affect host response to viral infections.
    Language English
    Publishing date 2017-02-20
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2587354-4
    ISSN 1664-302X
    ISSN 1664-302X
    DOI 10.3389/fmicb.2017.00240
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  9. Article ; Online: The microtubule-associated Rho activating factor GEF-H1 interacts with exocyst complex to regulate vesicle traffic.

    Pathak, Ritu / Delorme-Walker, Violaine D / Howell, Michael C / Anselmo, Anthony N / White, Michael A / Bokoch, Gary M / Dermardirossian, Céline

    Developmental cell

    2012  Volume 23, Issue 2, Page(s) 397–411

    Abstract: The exocyst complex plays a critical role in targeting and tethering vesicles to specific sites of the plasma membrane. These events are crucial for polarized delivery of membrane components to the cell surface, which is critical for cell motility and ... ...

    Abstract The exocyst complex plays a critical role in targeting and tethering vesicles to specific sites of the plasma membrane. These events are crucial for polarized delivery of membrane components to the cell surface, which is critical for cell motility and division. Though Rho GTPases are involved in regulating actin dynamics and membrane trafficking, their role in exocyst-mediated vesicle targeting is not very clear. Herein, we present evidence that depletion of GEF-H1, a guanine nucleotide exchange factor for Rho proteins, affects vesicle trafficking. Interestingly, we found that GEF-H1 directly binds to exocyst component Sec5 in a Ral GTPase-dependent manner. This interaction promotes RhoA activation, which then regulates exocyst assembly/localization and exocytosis. Taken together, our work defines a mechanism for RhoA activation in response to RalA-Sec5 signaling and involvement of GEF-H1/RhoA pathway in the regulation of vesicle trafficking.
    MeSH term(s) Biological Transport ; Enzyme Activation ; Exocytosis ; Guanine Nucleotide Exchange Factors/genetics ; Guanine Nucleotide Exchange Factors/metabolism ; HeLa Cells ; Humans ; Microscopy, Electron, Transmission ; Microtubules/metabolism ; Protein Binding ; Rho Guanine Nucleotide Exchange Factors ; Signal Transduction ; rhoA GTP-Binding Protein/metabolism
    Chemical Substances ARHGEF2 protein, human ; Guanine Nucleotide Exchange Factors ; Rho Guanine Nucleotide Exchange Factors ; rhoA GTP-Binding Protein (EC 3.6.5.2)
    Language English
    Publishing date 2012-08-17
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2054967-2
    ISSN 1878-1551 ; 1534-5807
    ISSN (online) 1878-1551
    ISSN 1534-5807
    DOI 10.1016/j.devcel.2012.06.014
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  10. Article ; Online: Recurrent hemizygous deletions in cancers may optimize proliferative potential.

    Solimini, Nicole L / Xu, Qikai / Mermel, Craig H / Liang, Anthony C / Schlabach, Michael R / Luo, Ji / Burrows, Anna E / Anselmo, Anthony N / Bredemeyer, Andrea L / Li, Mamie Z / Beroukhim, Rameen / Meyerson, Matthew / Elledge, Stephen J

    Science (New York, N.Y.)

    2012  Volume 337, Issue 6090, Page(s) 104–109

    Abstract: Tumors exhibit numerous recurrent hemizygous focal deletions that contain no known tumor suppressors and are poorly understood. To investigate whether these regions contribute to tumorigenesis, we searched genetically for genes with cancer-relevant ... ...

    Abstract Tumors exhibit numerous recurrent hemizygous focal deletions that contain no known tumor suppressors and are poorly understood. To investigate whether these regions contribute to tumorigenesis, we searched genetically for genes with cancer-relevant properties within these hemizygous deletions. We identified STOP and GO genes, which negatively and positively regulate proliferation, respectively. STOP genes include many known tumor suppressors, whereas GO genes are enriched for essential genes. Analysis of their chromosomal distribution revealed that recurring deletions preferentially overrepresent STOP genes and underrepresent GO genes. We propose a hypothesis called the cancer gene island model, whereby gene islands encompassing high densities of STOP genes and low densities of GO genes are hemizygously deleted to maximize proliferative fitness through cumulative haploinsufficiencies. Because hundreds to thousands of genes are hemizygously deleted per tumor, this mechanism may help to drive tumorigenesis across many cancer types.
    MeSH term(s) Cell Line ; Cell Line, Tumor ; Cell Proliferation ; Cell Transformation, Neoplastic ; Chromosome Mapping ; Genes, Essential ; Genes, Neoplasm ; Genes, Recessive ; Genes, Tumor Suppressor ; Haploinsufficiency ; Hemizygote ; Humans ; Models, Genetic ; Neoplasms/genetics ; Neoplasms/pathology ; Oncogenes ; Sequence Deletion
    Language English
    Publishing date 2012-05-24
    Publishing country United States
    Document type 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 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.1219580
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