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A bacterial effector protein promotes nuclear translocation of Stat3 to induce IL-10.

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A bacterial effector protein promotes nuclear translocation of Stat3 to induce IL-10. / Berneking, L; Bekere, I; Rob, S; Schnapp, M; Huang, J; Ruckdeschel, K; Aepfelbacher, M.

In: EUR J CELL BIOL, Vol. 102, No. 4, 151364, 12.2023, p. 151364.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Berneking, L, Bekere, I, Rob, S, Schnapp, M, Huang, J, Ruckdeschel, K & Aepfelbacher, M 2023, 'A bacterial effector protein promotes nuclear translocation of Stat3 to induce IL-10.', EUR J CELL BIOL, vol. 102, no. 4, 151364, pp. 151364. https://doi.org/10.1016/j.ejcb.2023.151364

APA

Berneking, L., Bekere, I., Rob, S., Schnapp, M., Huang, J., Ruckdeschel, K., & Aepfelbacher, M. (2023). A bacterial effector protein promotes nuclear translocation of Stat3 to induce IL-10. EUR J CELL BIOL, 102(4), 151364. [151364]. https://doi.org/10.1016/j.ejcb.2023.151364

Vancouver

Berneking L, Bekere I, Rob S, Schnapp M, Huang J, Ruckdeschel K et al. A bacterial effector protein promotes nuclear translocation of Stat3 to induce IL-10. EUR J CELL BIOL. 2023 Dec;102(4):151364. 151364. https://doi.org/10.1016/j.ejcb.2023.151364

Bibtex

@article{c1d64e689be44cfca56d74a33cccac91,
title = "A bacterial effector protein promotes nuclear translocation of Stat3 to induce IL-10.",
abstract = "The multifunctional Yersinia effector YopM inhibits effector triggered immunity and increases production of the anti-inflammatory cytokine Interleukin-10 (IL-10) to suppress the host immune response. Previously it was shown that YopM induces IL-10 gene expression by elevating phosphorylation of the serine-threonine kinase RSK1 in the nucleus of human macrophages. Using transcriptomics, we found that YopM strongly affects expression of genes belonging to the JAK-STAT signaling pathway. Further analysis revealed that YopM mediates nuclear translocation of the transcription factor Stat3 in Y. enterocolitica infected macrophages and that knockdown of Stat3 inhibited YopM-induced IL-10 gene expression. YopM-induced Stat3 translocation did not depend on autocrine IL-10, activation of RSK1 or tyrosine phosphorylation of Stat3. Thus, besides activation of RSK1, stimulation of nuclear translocation of Stat3 is another mechanism by which YopM increases IL-10 gene expression in macrophages.",
author = "L Berneking and I Bekere and S Rob and M Schnapp and J Huang and K Ruckdeschel and M Aepfelbacher",
year = "2023",
month = dec,
doi = "10.1016/j.ejcb.2023.151364",
language = "English",
volume = "102",
pages = "151364",
journal = "EUR J CELL BIOL",
issn = "0171-9335",
publisher = "Urban und Fischer Verlag GmbH und Co. KG",
number = "4",

}

RIS

TY - JOUR

T1 - A bacterial effector protein promotes nuclear translocation of Stat3 to induce IL-10.

AU - Berneking, L

AU - Bekere, I

AU - Rob, S

AU - Schnapp, M

AU - Huang, J

AU - Ruckdeschel, K

AU - Aepfelbacher, M

PY - 2023/12

Y1 - 2023/12

N2 - The multifunctional Yersinia effector YopM inhibits effector triggered immunity and increases production of the anti-inflammatory cytokine Interleukin-10 (IL-10) to suppress the host immune response. Previously it was shown that YopM induces IL-10 gene expression by elevating phosphorylation of the serine-threonine kinase RSK1 in the nucleus of human macrophages. Using transcriptomics, we found that YopM strongly affects expression of genes belonging to the JAK-STAT signaling pathway. Further analysis revealed that YopM mediates nuclear translocation of the transcription factor Stat3 in Y. enterocolitica infected macrophages and that knockdown of Stat3 inhibited YopM-induced IL-10 gene expression. YopM-induced Stat3 translocation did not depend on autocrine IL-10, activation of RSK1 or tyrosine phosphorylation of Stat3. Thus, besides activation of RSK1, stimulation of nuclear translocation of Stat3 is another mechanism by which YopM increases IL-10 gene expression in macrophages.

AB - The multifunctional Yersinia effector YopM inhibits effector triggered immunity and increases production of the anti-inflammatory cytokine Interleukin-10 (IL-10) to suppress the host immune response. Previously it was shown that YopM induces IL-10 gene expression by elevating phosphorylation of the serine-threonine kinase RSK1 in the nucleus of human macrophages. Using transcriptomics, we found that YopM strongly affects expression of genes belonging to the JAK-STAT signaling pathway. Further analysis revealed that YopM mediates nuclear translocation of the transcription factor Stat3 in Y. enterocolitica infected macrophages and that knockdown of Stat3 inhibited YopM-induced IL-10 gene expression. YopM-induced Stat3 translocation did not depend on autocrine IL-10, activation of RSK1 or tyrosine phosphorylation of Stat3. Thus, besides activation of RSK1, stimulation of nuclear translocation of Stat3 is another mechanism by which YopM increases IL-10 gene expression in macrophages.

UR - http://europepmc.org/abstract/med/37806297

U2 - 10.1016/j.ejcb.2023.151364

DO - 10.1016/j.ejcb.2023.151364

M3 - SCORING: Journal article

C2 - 37806297

VL - 102

SP - 151364

JO - EUR J CELL BIOL

JF - EUR J CELL BIOL

SN - 0171-9335

IS - 4

M1 - 151364

ER -