Central Role of ULK1 in Type I Interferon Signaling | Zendy

Diana Saleiro | Zendy; Swarna Mehrotra | Zendy; Barbara Kroczyńska | Zendy; Elspeth M. Beauchamp | Zendy; Paweł Lisowski | Zendy; Beata Majchrzak-Kita | Zendy; Tushar D. Bhagat | Zendy; Brady L. Stein | Zendy; Brandon McMahon | Zendy; Jessica K. Altman | Zendy; Ewa M. Kościuczuk | Zendy; Darren P. Baker | Zendy; Chunfa Jie | Zendy; Nadereh Jafari | Zendy; Craig B. Thompson | Zendy; Ross L. Levine | Zendy; Eleanor N. Fish | Zendy; Amit Verma | Zendy; Leonidas C. Platanias | Zendy

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Central Role of ULK1 in Type I Interferon Signaling

Author(s) -

Diana Saleiro,

Swarna Mehrotra,

Barbara Kroczyńska,

Elspeth M. Beauchamp,

Paweł Lisowski,

Beata Majchrzak-Kita,

Tushar D. Bhagat,

Brady L. Stein,

Brandon McMahon,

Jessica K. Altman,

Ewa M. Kościuczuk,

Darren P. Baker,

Chunfa Jie,

Nadereh Jafari,

Craig B. Thompson,

Ross L. Levine,

Eleanor N. Fish,

Amit Verma,

Leonidas C. Platanias

Publication year - 2015

Publication title -

cell reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 6.264

H-Index - 154

eISSN - 2639-1856

pISSN - 2211-1247

DOI - 10.1016/j.celrep.2015.03.056

Subject(s) - ulk1 , interferon , biology , protein kinase a , cancer research , transcription factor , microbiology and biotechnology , mediator , regulator , mapk/erk pathway , p38 mitogen activated protein kinases , kinase , signal transduction , gene , immunology , genetics , ampk

We provide evidence that the Unc-51-like kinase 1 (ULK1) is activated during engagement of the type I interferon (IFN) receptor (IFNR). Our studies demonstrate that the function of ULK1 is required for gene transcription mediated via IFN-stimulated response elements (ISRE) and IFNγ activation site (GAS) elements and controls expression of key IFN-stimulated genes (ISGs). We identify ULK1 as an upstream regulator of p38α mitogen-activated protein kinase (MAPK) and establish that the regulatory effects of ULK1 on ISG expression are mediated possibly by engagement of the p38 MAPK pathway. Importantly, we demonstrate that ULK1 is essential for antiproliferative responses and type I IFN-induced antineoplastic effects against malignant erythroid precursors from patients with myeloproliferative neoplasms. Together, these data reveal a role for ULK1 as a key mediator of type I IFNR-generated signals that control gene transcription and induction of antineoplastic responses.

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