Publication

The PI3K and MAPK/p38 pathways control stress granule assembly in a hierarchical manner

Heberle, A. M., Razquin Navas, P., Langelaar-Makkinje, M., Kasack, K., Sadik, A., Faessler, E., Hahn, U., Marx-Stoelting, P., Opitz, C. A., Sers, C., Heiland, I., Schäuble, S. & Thedieck, K., Apr-2019, In : Life science alliance. 2, 2, 22 p., 201800257.

Research output: Contribution to journalArticleAcademicpeer-review

APA

Heberle, A. M., Razquin Navas, P., Langelaar-Makkinje, M., Kasack, K., Sadik, A., Faessler, E., Hahn, U., Marx-Stoelting, P., Opitz, C. A., Sers, C., Heiland, I., Schäuble, S., & Thedieck, K. (2019). The PI3K and MAPK/p38 pathways control stress granule assembly in a hierarchical manner. Life science alliance, 2(2), [201800257]. https://doi.org/10.26508/lsa.201800257

Author

Heberle, Alexander Martin ; Razquin Navas, Patricia ; Langelaar-Makkinje, Miriam ; Kasack, Katharina ; Sadik, Ahmed ; Faessler, Erik ; Hahn, Udo ; Marx-Stoelting, Philip ; Opitz, Christiane A ; Sers, Christine ; Heiland, Ines ; Schäuble, Sascha ; Thedieck, Kathrin. / The PI3K and MAPK/p38 pathways control stress granule assembly in a hierarchical manner. In: Life science alliance. 2019 ; Vol. 2, No. 2.

Harvard

Heberle, AM, Razquin Navas, P, Langelaar-Makkinje, M, Kasack, K, Sadik, A, Faessler, E, Hahn, U, Marx-Stoelting, P, Opitz, CA, Sers, C, Heiland, I, Schäuble, S & Thedieck, K 2019, 'The PI3K and MAPK/p38 pathways control stress granule assembly in a hierarchical manner', Life science alliance, vol. 2, no. 2, 201800257. https://doi.org/10.26508/lsa.201800257

Standard

The PI3K and MAPK/p38 pathways control stress granule assembly in a hierarchical manner. / Heberle, Alexander Martin; Razquin Navas, Patricia; Langelaar-Makkinje, Miriam; Kasack, Katharina; Sadik, Ahmed; Faessler, Erik; Hahn, Udo; Marx-Stoelting, Philip; Opitz, Christiane A; Sers, Christine; Heiland, Ines; Schäuble, Sascha; Thedieck, Kathrin.

In: Life science alliance, Vol. 2, No. 2, 201800257, 04.2019.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

Heberle AM, Razquin Navas P, Langelaar-Makkinje M, Kasack K, Sadik A, Faessler E et al. The PI3K and MAPK/p38 pathways control stress granule assembly in a hierarchical manner. Life science alliance. 2019 Apr;2(2). 201800257. https://doi.org/10.26508/lsa.201800257


BibTeX

@article{a3f4007242d540c5b9704cf312386b37,
title = "The PI3K and MAPK/p38 pathways control stress granule assembly in a hierarchical manner",
abstract = "All cells and organisms exhibit stress-coping mechanisms to ensure survival. Cytoplasmic protein-RNA assemblies termed stress granules are increasingly recognized to promote cellular survival under stress. Thus, they might represent tumor vulnerabilities that are currently poorly explored. The translation-inhibitory eIF2α kinases are established as main drivers of stress granule assembly. Using a systems approach, we identify the translation enhancers PI3K and MAPK/p38 as pro-stress-granule-kinases. They act through the metabolic master regulator mammalian target of rapamycin complex 1 (mTORC1) to promote stress granule assembly. When highly active, PI3K is the main driver of stress granules; however, the impact of p38 becomes apparent as PI3K activity declines. PI3K and p38 thus act in a hierarchical manner to drive mTORC1 activity and stress granule assembly. Of note, this signaling hierarchy is also present in human breast cancer tissue. Importantly, only the recognition of the PI3K-p38 hierarchy under stress enabled the discovery of p38's role in stress granule formation. In summary, we assign a new pro-survival function to the key oncogenic kinases PI3K and p38, as they hierarchically promote stress granule formation.",
author = "Heberle, {Alexander Martin} and {Razquin Navas}, Patricia and Miriam Langelaar-Makkinje and Katharina Kasack and Ahmed Sadik and Erik Faessler and Udo Hahn and Philip Marx-Stoelting and Opitz, {Christiane A} and Christine Sers and Ines Heiland and Sascha Sch{\"a}uble and Kathrin Thedieck",
note = "{\textcopyright} 2019 Heberle et al.",
year = "2019",
month = apr,
doi = "10.26508/lsa.201800257",
language = "English",
volume = "2",
journal = "Life science alliance",
issn = "2575-1077",
publisher = "Life Science Alliance LLC",
number = "2",

}

RIS

TY - JOUR

T1 - The PI3K and MAPK/p38 pathways control stress granule assembly in a hierarchical manner

AU - Heberle, Alexander Martin

AU - Razquin Navas, Patricia

AU - Langelaar-Makkinje, Miriam

AU - Kasack, Katharina

AU - Sadik, Ahmed

AU - Faessler, Erik

AU - Hahn, Udo

AU - Marx-Stoelting, Philip

AU - Opitz, Christiane A

AU - Sers, Christine

AU - Heiland, Ines

AU - Schäuble, Sascha

AU - Thedieck, Kathrin

N1 - © 2019 Heberle et al.

PY - 2019/4

Y1 - 2019/4

N2 - All cells and organisms exhibit stress-coping mechanisms to ensure survival. Cytoplasmic protein-RNA assemblies termed stress granules are increasingly recognized to promote cellular survival under stress. Thus, they might represent tumor vulnerabilities that are currently poorly explored. The translation-inhibitory eIF2α kinases are established as main drivers of stress granule assembly. Using a systems approach, we identify the translation enhancers PI3K and MAPK/p38 as pro-stress-granule-kinases. They act through the metabolic master regulator mammalian target of rapamycin complex 1 (mTORC1) to promote stress granule assembly. When highly active, PI3K is the main driver of stress granules; however, the impact of p38 becomes apparent as PI3K activity declines. PI3K and p38 thus act in a hierarchical manner to drive mTORC1 activity and stress granule assembly. Of note, this signaling hierarchy is also present in human breast cancer tissue. Importantly, only the recognition of the PI3K-p38 hierarchy under stress enabled the discovery of p38's role in stress granule formation. In summary, we assign a new pro-survival function to the key oncogenic kinases PI3K and p38, as they hierarchically promote stress granule formation.

AB - All cells and organisms exhibit stress-coping mechanisms to ensure survival. Cytoplasmic protein-RNA assemblies termed stress granules are increasingly recognized to promote cellular survival under stress. Thus, they might represent tumor vulnerabilities that are currently poorly explored. The translation-inhibitory eIF2α kinases are established as main drivers of stress granule assembly. Using a systems approach, we identify the translation enhancers PI3K and MAPK/p38 as pro-stress-granule-kinases. They act through the metabolic master regulator mammalian target of rapamycin complex 1 (mTORC1) to promote stress granule assembly. When highly active, PI3K is the main driver of stress granules; however, the impact of p38 becomes apparent as PI3K activity declines. PI3K and p38 thus act in a hierarchical manner to drive mTORC1 activity and stress granule assembly. Of note, this signaling hierarchy is also present in human breast cancer tissue. Importantly, only the recognition of the PI3K-p38 hierarchy under stress enabled the discovery of p38's role in stress granule formation. In summary, we assign a new pro-survival function to the key oncogenic kinases PI3K and p38, as they hierarchically promote stress granule formation.

U2 - 10.26508/lsa.201800257

DO - 10.26508/lsa.201800257

M3 - Article

C2 - 30923191

VL - 2

JO - Life science alliance

JF - Life science alliance

SN - 2575-1077

IS - 2

M1 - 201800257

ER -

ID: 79555564