Innate immune and proinflammatory signals activate the Hippo pathway via a Tak1-STRIPAK-Tao axis
© 2024. The Author(s)..
The Hippo pathway controls developmental, homeostatic and regenerative tissue growth, and is frequently dysregulated in various diseases. Although this pathway can be activated by innate immune/inflammatory stimuli, the underlying mechanism is not fully understood. Here, we identify a conserved signaling cascade that leads to Hippo pathway activation by innate immune/inflammatory signals. We show that Tak1, a key kinase in innate immune/inflammatory signaling, activates the Hippo pathway by inducing the lysosomal degradation of Cka, an essential subunit of the STRIPAK PP2A complex that suppresses Hippo signaling. Suppression of STRIPAK results in the activation of Hippo pathway through Tao-Hpo signaling. We further show that Tak1-mediated Hippo signaling is involved in processes ranging from cell death to phagocytosis and innate immune memory. Our findings thus reveal a molecular connection between innate immune/inflammatory signaling and the evolutionally conserved Hippo pathway, thus contributing to our understanding of infectious, inflammatory and malignant diseases.
Medienart: |
E-Artikel |
---|
Erscheinungsjahr: |
2024 |
---|---|
Erschienen: |
2024 |
Enthalten in: |
Zur Gesamtaufnahme - volume:15 |
---|---|
Enthalten in: |
Nature communications - 15(2024), 1 vom: 02. Jan., Seite 145 |
Sprache: |
Englisch |
---|
Beteiligte Personen: |
Yang, Yinan [VerfasserIn] |
---|
Links: |
---|
Themen: |
---|
Anmerkungen: |
Date Completed 05.01.2024 Date Revised 10.02.2024 published: Electronic Citation Status MEDLINE |
---|
doi: |
10.1038/s41467-023-44542-y |
---|
funding: |
|
---|---|
Förderinstitution / Projekttitel: |
|
PPN (Katalog-ID): |
NLM366587080 |
---|
LEADER | 01000caa a22002652 4500 | ||
---|---|---|---|
001 | NLM366587080 | ||
003 | DE-627 | ||
005 | 20240210233038.0 | ||
007 | cr uuu---uuuuu | ||
008 | 240108s2024 xx |||||o 00| ||eng c | ||
024 | 7 | |a 10.1038/s41467-023-44542-y |2 doi | |
028 | 5 | 2 | |a pubmed24n1287.xml |
035 | |a (DE-627)NLM366587080 | ||
035 | |a (NLM)38168080 | ||
040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
041 | |a eng | ||
100 | 1 | |a Yang, Yinan |e verfasserin |4 aut | |
245 | 1 | 0 | |a Innate immune and proinflammatory signals activate the Hippo pathway via a Tak1-STRIPAK-Tao axis |
264 | 1 | |c 2024 | |
336 | |a Text |b txt |2 rdacontent | ||
337 | |a ƒaComputermedien |b c |2 rdamedia | ||
338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
500 | |a Date Completed 05.01.2024 | ||
500 | |a Date Revised 10.02.2024 | ||
500 | |a published: Electronic | ||
500 | |a Citation Status MEDLINE | ||
520 | |a © 2024. The Author(s). | ||
520 | |a The Hippo pathway controls developmental, homeostatic and regenerative tissue growth, and is frequently dysregulated in various diseases. Although this pathway can be activated by innate immune/inflammatory stimuli, the underlying mechanism is not fully understood. Here, we identify a conserved signaling cascade that leads to Hippo pathway activation by innate immune/inflammatory signals. We show that Tak1, a key kinase in innate immune/inflammatory signaling, activates the Hippo pathway by inducing the lysosomal degradation of Cka, an essential subunit of the STRIPAK PP2A complex that suppresses Hippo signaling. Suppression of STRIPAK results in the activation of Hippo pathway through Tao-Hpo signaling. We further show that Tak1-mediated Hippo signaling is involved in processes ranging from cell death to phagocytosis and innate immune memory. Our findings thus reveal a molecular connection between innate immune/inflammatory signaling and the evolutionally conserved Hippo pathway, thus contributing to our understanding of infectious, inflammatory and malignant diseases | ||
650 | 4 | |a Journal Article | |
650 | 7 | |a Protein Serine-Threonine Kinases |2 NLM | |
650 | 7 | |a EC 2.7.11.1 |2 NLM | |
700 | 1 | |a Zhou, Huijing |e verfasserin |4 aut | |
700 | 1 | |a Huang, Xiawei |e verfasserin |4 aut | |
700 | 1 | |a Wu, Chengfang |e verfasserin |4 aut | |
700 | 1 | |a Zheng, Kewei |e verfasserin |4 aut | |
700 | 1 | |a Deng, Jingrong |e verfasserin |4 aut | |
700 | 1 | |a Zheng, Yonggang |e verfasserin |4 aut | |
700 | 1 | |a Wang, Jiahui |e verfasserin |4 aut | |
700 | 1 | |a Chi, Xiaofeng |e verfasserin |4 aut | |
700 | 1 | |a Ma, Xianjue |e verfasserin |4 aut | |
700 | 1 | |a Pan, Huimin |e verfasserin |4 aut | |
700 | 1 | |a Shen, Rui |e verfasserin |4 aut | |
700 | 1 | |a Pan, Duojia |e verfasserin |4 aut | |
700 | 1 | |a Liu, Bo |e verfasserin |4 aut | |
773 | 0 | 8 | |i Enthalten in |t Nature communications |d 2010 |g 15(2024), 1 vom: 02. Jan., Seite 145 |w (DE-627)NLM199274525 |x 2041-1723 |7 nnns |
773 | 1 | 8 | |g volume:15 |g year:2024 |g number:1 |g day:02 |g month:01 |g pages:145 |
856 | 4 | 0 | |u http://dx.doi.org/10.1038/s41467-023-44542-y |3 Volltext |
912 | |a GBV_USEFLAG_A | ||
912 | |a GBV_NLM | ||
951 | |a AR | ||
952 | |d 15 |j 2024 |e 1 |b 02 |c 01 |h 145 |