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An alternatively transcribed TAZ variant negatively regulates JAK ‐ STAT signaling
Author(s) -
Fang Chuantao,
Li Jian,
Qi Sixian,
Lei Yubin,
Zeng Yan,
Yu Pengcheng,
Hu Zhaolan,
Zhou Yufeng,
Wang Yulong,
Dai Ruping,
Li Jin,
Huang Shenglin,
Xu Pinglong,
Chen Kang,
Ding Chen,
Yu FaXing
Publication year - 2019
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.15252/embr.201847227
Subject(s) - stat , signal transduction , microbiology and biotechnology , biology , stat3
Type I interferon ( IFN )‐induced Janus kinase ( JAK )–signal transducer and activator of transcription ( STAT ) signaling drives the expression of IFN ‐stimulated genes ( ISG s) to mediate antiviral response. The strength and duration of JAK ‐ STAT signaling are tightly regulated to ensure effective antiviral defense while avoiding pathological inflammation and autoimmunity. Here, we report that cTAZ , an isoform of the Hippo pathway effector TAZ , is transcribed by an alternative promoter. Although majority of C‐terminal sequences of TAZ is retained, cTAZ is not regulated by the Hippo signaling and does not mediate its growth‐inhibitory functions. Instead, cTAZ negatively regulates JAK ‐ STAT signaling by inhibiting STAT 1/2 nuclear localization and ISG expression, and its expression is induced by type I IFN . Thus, cTAZ functions as a modulator of JAK ‐ STAT signaling and may play a role in fine‐tuning cellular antiviral response.