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Paper Details

Tumor suppressor cylindromatosis (CYLD) controls HIV transcription in an NF-κB-dependent manner.
J Virol
22
2014
CD4, CD4(, CD4(+, CD4(+), CD4(+) T cells, CD4(+) T lymphocytes, CYLD, CYLD protein, HIV, HIV long terminal repeat, HIV mRNA, JLat cells, Jurkat T cells, LTR, NF-B, PMA, T cell lines, T cells, Tumor, cylindromatosis, cylindromatosis protein, dendritic cells, deubiquitinase, human, lysine, lysine 63 deubiquitinase, monocyte-derived macrophages, phorbol 12-myristate 13-acetate, primary CD4(+), primary human CD4(+) T cells, small interfering RNA, target cells, transformed T cell lines
Author NameAffiliation
Lara ManganaroIcahn School of Medicine at Mount Sinai
Lars PacheSanford-Burnham Medical Research Institute
John MarlettNomis Center for Immunobiology and Microbial Pathogenesis, The Salk Institute for Biological Studies
Lisa MiorinIcahn School of Medicine at Mount Sinai
Adrian T TingImmunology Institute, Icahn School of Medicine at Mount Sinai
Renate K??nigSanford-Burnham Medical Research Institute, USA Research Group "Host-Pathogen Interactions," Paul-Ehrlich-Institut
Adolfo Garc??a-SastreIcahn School of Medicine at Mount Sinai, USA Global Health and Emerging Pathogens Institute
Frederic D BushmanPerelman School of Medicine at the University of Pennsylvania
Sumit K ChandaSanford-Burnham Medical Research Institute
John A T YoungNomis Center for Immunobiology and Microbial Pathogenesis, The Salk Institute for Biological Studies
Ana Fernandez-SesmaIcahn School of Medicine at Mount Sinai
Viviana SimonIcahn School of Medicine at Mount Sinai, USA Global Health and Emerging Pathogens Institute
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