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  • 1
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    Antiapoptotic protein Lifeguard is required for survival and maintenance of Purkinje and granular cells [Neuroscience] (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-10-12
    Description: Lifeguard (LFG) is an inhibitor of Fas-mediated cell death and is highly expressed in the cerebellum. We investigated the biological role of LFG in the cerebellum in vivo, using mice with reduced LFG expression generated by shRNA lentiviral transgenesis (shLFG mice) as well as LFG null mice. We found that LFG plays a role in cerebellar development by affecting cerebellar size, internal granular layer (IGL) thickness, and Purkinje cell (PC) development. All these features are more severe in early developmental stages and show substantial recovery overtime, providing a remarkable example of cerebellar plasticity. In adult mice, LFG plays a role in PC maintenance shown by reduced cellular density and abnormal morphology with increased active caspase 8 and caspase 3 immunostaining in shLFG and knockout (KO) PCs. We studied the mechanism of action of LFG as an inhibitor of the Fas pathway and provided evidence of the neuroprotective role of LFG in cerebellar granule neurons (CGNs) and PCs in an organotypic cerebellar culture system. Biochemical analysis of the Fas pathway revealed that LFG inhibits Fas-mediated cell death by interfering with caspase 8 activation. This result is supported by the increased number of active caspase 8-positive PCs in adult mice lacking LFG. These data demonstrate that LFG is required for proper development and survival of granular and Purkinje cells and suggest LFG may play a role in cerebellar disorders.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 2
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    Role of BRCA1 in brain development [Cell Biology] (2014)
    National Academy of Sciences
    Details
    Publication Date: 2014-04-02
    Description: Breast cancer susceptibility gene 1 (BRCA1) is a breast and ovarian cancer tumor suppressor whose loss leads to DNA damage and defective centrosome functions. Despite its tumor suppression functions, BRCA1 is most highly expressed in the embryonic neuroepithelium when the neural progenitors are highly proliferative. To determine its functional significance,...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 3
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    Tumor suppressor protein (p)53, is a regulator of NF-{kappa}B repression by the glucocorticoid receptor [Medical Sciences] (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-10-12
    Description: Glucocorticoids can inhibit inflammation by abrogating the activity of NF-κB, a family of transcription factors that regulates the production of proinflammatory cytokines. To understand the molecular mechanism of repression of NF-κB activity by glucocorticoids, we performed a high-throughput siRNA oligo screen to identify novel genes involved in this process. Here, we report that loss of p53, a tumor suppressor protein, impaired repression of NF-κB target gene transcription by glucocorticoids. Additionally, loss of p53 also impaired transcription of glucocorticoid receptor (GR) target genes, whereas upstream NF-κB and glucocorticoid receptor signaling cascades remained intact. We further demonstrate that p53 loss severely impaired glucocorticoid rescue of death in a mouse model of LPS shock. Our findings unveil a new role for p53 in the repression of NF-κB by glucocorticoids and suggest important implications for treatment of the proinflammatory microenvironments found in tumors with aberrant p53 activity.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 4
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    Severe liver degeneration in mice lacking the IkappaB kinase 2 gene (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-09
    Description: Phosphorylation of inhibitor of kappa B (IkappaB) proteins is an important step in the activation of the transcription nuclear factor kappa B (NF-kappaB) and requires two IkappaB kinases, IKK1 (IKKalpha) and IKK2 (IKKbeta). Mice that are devoid of the IKK2 gene had extensive liver damage from apoptosis and died as embryos, but these mice could be rescued by the inactivation of the gene encoding tumor necrosis factor receptor 1. Mouse embryonic fibroblast cells that were isolated from IKK2-/- embryos showed a marked reduction in tumor necrosis factor-alpha (TNF-alpha)- and interleukin-1alpha-induced NF-kappaB activity and an enhanced apoptosis in response to TNF-alpha. IKK1 associated with NF-kappaB essential modulator (IKKgamma/IKKAP1), another component of the IKK complex. These results show that IKK2 is essential for mouse development and cannot be substituted with IKK1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Q -- Van Antwerp, D -- Mercurio, F -- Lee, K F -- Verma, I M -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):321-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Salk Institute, La Jolla, CA 92037, USA. Signal Pharmaceuticals, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10195897" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Line ; DNA-Binding Proteins/metabolism ; Embryonic and Fetal Development ; Gene Targeting ; I-kappa B Kinase ; I-kappa B Proteins ; Interleukin-1/pharmacology ; Liver/cytology/*embryology ; Mice ; NF-kappa B/metabolism ; Phosphorylation ; Polymerase Chain Reaction ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Receptors, Tumor Necrosis Factor/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Sequence Deletion ; Signal Transduction ; Transcription Factor RelA ; Transcription Factors/metabolism ; Tumor Necrosis Factor-alpha/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 5
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    Transduction of human CD34+ cells that mediate long-term engraftment of NOD/SCID mice by HIV vectors (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-29
    Description: Efficient gene transfer into human hematopoietic stem cells (HSCs) is an important goal in the study of the hematopoietic system as well as for gene therapy of hematopoietic disorders. A lentiviral vector based on the human immunodeficiency virus (HIV) was able to transduce human CD34+ cells capable of stable, long-term reconstitution of nonobese diabetic/severe combined immunodeficient (NOD/SCID) mice. High-efficiency transduction occurred in the absence of cytokine stimulation and resulted in transgene expression in multiple lineages of human hematopoietic cells for up to 22 weeks after transplantation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyoshi, H -- Smith, K A -- Mosier, D E -- Verma, I M -- Torbett, B E -- CA44360/CA/NCI NIH HHS/ -- DK49886/DK/NIDDK NIH HHS/ -- HL53670/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 29;283(5402):682-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9924027" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD34/*analysis ; Bone Marrow Cells/cytology ; Cell Division ; Cell Survival ; Colony-Forming Units Assay ; Gene Expression ; *Gene Transfer Techniques ; *Genetic Vectors ; Green Fluorescent Proteins ; HIV/*genetics ; Hematopoiesis ; *Hematopoietic Stem Cell Transplantation ; *Hematopoietic Stem Cells/cytology/immunology ; Humans ; Leukemia Virus, Murine/genetics ; Luminescent Proteins/genetics ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Promoter Regions, Genetic ; Transfection ; Transgenes
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Disease-corrected haematopoietic progenitors from Fanconi anaemia induced pluripotent stem cells (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-06-02
    Description: The generation of induced pluripotent stem (iPS) cells has enabled the derivation of patient-specific pluripotent cells and provided valuable experimental platforms to model human disease. Patient-specific iPS cells are also thought to hold great therapeutic potential, although direct evidence for this is still lacking. Here we show that, on correction of the genetic defect, somatic cells from Fanconi anaemia patients can be reprogrammed to pluripotency to generate patient-specific iPS cells. These cell lines appear indistinguishable from human embryonic stem cells and iPS cells from healthy individuals. Most importantly, we show that corrected Fanconi-anaemia-specific iPS cells can give rise to haematopoietic progenitors of the myeloid and erythroid lineages that are phenotypically normal, that is, disease-free. These data offer proof-of-concept that iPS cell technology can be used for the generation of disease-corrected, patient-specific cells with potential value for cell therapy applications.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2720823/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2720823/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raya, Angel -- Rodriguez-Piza, Ignasi -- Guenechea, Guillermo -- Vassena, Rita -- Navarro, Susana -- Barrero, Maria Jose -- Consiglio, Antonella -- Castella, Maria -- Rio, Paula -- Sleep, Eduard -- Gonzalez, Federico -- Tiscornia, Gustavo -- Garreta, Elena -- Aasen, Trond -- Veiga, Anna -- Verma, Inder M -- Surralles, Jordi -- Bueren, Juan -- Izpisua Belmonte, Juan Carlos -- R01 HL053670/HL/NHLBI NIH HHS/ -- R01 HL053670-14/HL/NHLBI NIH HHS/ -- England -- Nature. 2009 Jul 2;460(7251):53-9. doi: 10.1038/nature08129. Epub 2009 May 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Regenerative Medicine in Barcelona, Dr. Aiguader 88, 08003 Barcelona, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19483674" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cellular Reprogramming ; Fanconi Anemia/*pathology/*therapy ; Health ; Hematopoietic Stem Cells/*cytology/metabolism ; Humans ; Pluripotent Stem Cells/*cytology/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 7
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    Dedifferentiation of neurons and astrocytes by oncogenes can induce gliomas in mice (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-10-23
    Description: Glioblastoma multiforme (GBM) is the most common and aggressive malignant primary brain tumor in humans. Here we show that gliomas can originate from differentiated cells in the central nervous system (CNS), including cortical neurons. Transduction by oncogenic lentiviral vectors of neural stem cells (NSCs), astrocytes, or even mature neurons in the brains of mice can give rise to malignant gliomas. All the tumors, irrespective of the site of lentiviral vector injection (the initiating population), shared common features of high expression of stem or progenitor markers and low expression of differentiation markers. Microarray analysis revealed that tumors of astrocytic and neuronal origin match the mesenchymal GBM subtype. We propose that most differentiated cells in the CNS upon defined genetic alterations undergo dedifferentiation to generate a NSC or progenitor state to initiate and maintain the tumor progression, as well as to give rise to the heterogeneous populations observed in malignant gliomas.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3595315/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3595315/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Friedmann-Morvinski, Dinorah -- Bushong, Eric A -- Ke, Eugene -- Soda, Yasushi -- Marumoto, Tomotoshi -- Singer, Oded -- Ellisman, Mark H -- Verma, Inder M -- 5P41RR004050/RR/NCRR NIH HHS/ -- HL053670/HL/NHLBI NIH HHS/ -- P30 CA014195/CA/NCI NIH HHS/ -- P30 CA014195-38/CA/NCI NIH HHS/ -- R01 HL053670/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2012 Nov 23;338(6110):1080-4. doi: 10.1126/science.1226929. Epub 2012 Oct 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23087000" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/metabolism/*pathology ; Brain Neoplasms/*genetics/*pathology ; Genes, Neurofibromatosis 1 ; Genes, p53 ; Glioblastoma/genetics/pathology ; Glioma/*genetics/*pathology ; Lentivirus ; Mice ; Mice, Transgenic ; Nerve Tissue Proteins/genetics ; Neural Stem Cells/metabolism/pathology ; Neurons/metabolism/*pathology ; *Oncogenes ; Transduction, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Activation of transcription factor NF-kappaB requires ELKS, an IkappaB kinase regulatory subunit (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-06-26
    Description: The nuclear factor-kappa B (NF-kappaB) family of transcription factors plays a seminal role in inflammation, apoptosis, development, and cancer. Modulation of NF-kappaB-mediated gene expression in response to diverse signals is coordinated by the IkappaB kinase (IKK) complex. We identified ELKS, an essential regulatory subunit of the IKK complex. Silencing ELKS expression by RNA interference blocked induced expression of NF-kappaB target genes, including the NF-kappaB inhibitor IkappaBalpha and proinflammatory genes such as cyclo-oxygenase 2 and interleukin 8. These cells were also not protected from apoptosis in response to cytokines. ELKS likely functions by recruiting IkappaBalpha to the IKK complex and thus serves a regulatory function for IKK activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ducut Sigala, Jeanette L -- Bottero, Virginie -- Young, David B -- Shevchenko, Andrej -- Mercurio, Frank -- Verma, Inder M -- New York, N.Y. -- Science. 2004 Jun 25;304(5679):1963-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Salk Institute for Biological Sciences, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15218148" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Apoptosis ; Carrier Proteins/genetics/*metabolism ; Cell Line ; Cyclooxygenase 2 ; Gene Expression ; Genes, Reporter ; HeLa Cells ; Humans ; I-kappa B Kinase ; I-kappa B Proteins/genetics/metabolism ; Interleukin-1/pharmacology ; Interleukin-8/genetics ; Isoenzymes/genetics ; Membrane Proteins ; Mice ; Mice, Knockout ; Mitogen-Activated Protein Kinases/metabolism ; Mutation ; NF-kappa B/*metabolism ; Nerve Tissue Proteins/genetics/*metabolism ; Phosphorylation ; Precipitin Tests ; Prostaglandin-Endoperoxide Synthases/genetics ; Protein-Serine-Threonine Kinases/*metabolism ; RNA Interference ; Tumor Necrosis Factor-alpha/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    BRCA1 tumour suppression occurs via heterochromatin-mediated silencing (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-09-09
    Description: Mutations in the tumour suppressor gene BRCA1 lead to breast and/or ovarian cancer. Here we show that loss of Brca1 in mice results in transcriptional de-repression of the tandemly repeated satellite DNA. Brca1 deficiency is accompanied by a reduction of condensed DNA regions in the genome and loss of ubiquitylation of histone H2A at satellite repeats. BRCA1 binds to satellite DNA regions and ubiquitylates H2A in vivo. Ectopic expression of H2A fused to ubiquitin reverses the effects of BRCA1 loss, indicating that BRCA1 maintains heterochromatin structure via ubiquitylation of histone H2A. Satellite DNA de-repression was also observed in mouse and human BRCA1-deficient breast cancers. Ectopic expression of satellite DNA can phenocopy BRCA1 loss in centrosome amplification, cell-cycle checkpoint defects, DNA damage and genomic instability. We propose that the role of BRCA1 in maintaining global heterochromatin integrity accounts for many of its tumour suppressor functions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240576/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240576/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhu, Quan -- Pao, Gerald M -- Huynh, Alexis M -- Suh, Hoonkyo -- Tonnu, Nina -- Nederlof, Petra M -- Gage, Fred H -- Verma, Inder M -- NS50217/NS/NINDS NIH HHS/ -- NS52842/NS/NINDS NIH HHS/ -- R01 NS050217/NS/NINDS NIH HHS/ -- R01 NS050217-05/NS/NINDS NIH HHS/ -- R01 NS052842/NS/NINDS NIH HHS/ -- R01 NS052842-04/NS/NINDS NIH HHS/ -- England -- Nature. 2011 Sep 7;477(7363):179-84. doi: 10.1038/nature10371.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21901007" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; BRCA1 Protein/deficiency/genetics/*metabolism ; Breast/cytology ; Breast Neoplasms/*genetics/pathology ; Cell Line, Tumor ; Cells, Cultured ; DNA, Satellite/genetics ; Epithelial Cells/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; *Gene Silencing ; Genes, BRCA1/*physiology ; Genomic Instability/genetics ; HeLa Cells ; Heterochromatin/*genetics/*metabolism ; Histones/metabolism ; Humans ; Mice ; Ovarian Neoplasms/genetics ; RNA, Messenger/genetics ; Transcription, Genetic/genetics ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitinated Proteins/metabolism ; Ubiquitination
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 10
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    Renato Dulbecco (1914-2012) (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-03-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Verma, Inder M -- England -- Nature. 2012 Mar 21;483(7390):408. doi: 10.1038/483408a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Salk Institute, La Jolla, California 92037, USA. verma@salk.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22437605" target="_blank"〉PubMed〈/a〉
    Keywords: Genes, Viral/genetics ; History, 20th Century ; Human Genome Project/history ; Italy ; Molecular Biology/*history ; Neoplasms/genetics/pathology/virology ; Nobel Prize ; United States ; Viral Plaque Assay/history
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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