Moonlighting chromatin: when DNA escapes nuclear control

Standard

Moonlighting chromatin: when DNA escapes nuclear control. / Singh, Jeeshan; Boettcher, Michael; Dölling, Maximilian; Heuer, Annika; Hohberger, Bettina; Leppkes, Moritz; Naschberger, Elisabeth; Schapher, Mirco; Schauer, Christine; Schoen, Janina; Stürzl, Michael; Vitkov, Ljubomir; Wang, Han; Zlatar, Leticija; Schett, Georg A.; Pisetsky, David S.; Liu, Ming-Lin; Herrmann, Martin; Knopf, Jasmin.

In: Cell death and differentiation, Vol. 30, No. 4, 04.2023, p. 861-875.

Research output: SCORING: Contribution to journalSCORING: Review articleResearch

Harvard

Singh, J, Boettcher, M, Dölling, M, Heuer, A, Hohberger, B, Leppkes, M, Naschberger, E, Schapher, M, Schauer, C, Schoen, J, Stürzl, M, Vitkov, L, Wang, H, Zlatar, L, Schett, GA, Pisetsky, DS, Liu, M-L, Herrmann, M & Knopf, J 2023, 'Moonlighting chromatin: when DNA escapes nuclear control', Cell death and differentiation, vol. 30, no. 4, pp. 861-875. https://doi.org/10.1038/s41418-023-01124-1

APA

Singh, J., Boettcher, M., Dölling, M., Heuer, A., Hohberger, B., Leppkes, M., Naschberger, E., Schapher, M., Schauer, C., Schoen, J., Stürzl, M., Vitkov, L., Wang, H., Zlatar, L., Schett, G. A., Pisetsky, D. S., Liu, M-L., Herrmann, M., & Knopf, J. (2023). Moonlighting chromatin: when DNA escapes nuclear control. Cell death and differentiation, 30(4), 861-875. https://doi.org/10.1038/s41418-023-01124-1

Vancouver

Singh J, Boettcher M, Dölling M, Heuer A, Hohberger B, Leppkes M et al. Moonlighting chromatin: when DNA escapes nuclear control. Cell death and differentiation. 2023 Apr;30(4):861-875. https://doi.org/10.1038/s41418-023-01124-1

Bibtex

@article{7a09d84294464bdba420e7ca23c19032,
title = "Moonlighting chromatin: when DNA escapes nuclear control",
abstract = "Extracellular chromatin, for example in the form of neutrophil extracellular traps (NETs), is an important element that propels the pathological progression of a plethora of diseases. DNA drives the interferon system, serves as autoantigen, and forms the extracellular scaffold for proteins of the innate immune system. An insufficient clearance of extruded chromatin after the release of DNA from the nucleus into the extracellular milieu can perform a secret task of moonlighting in immune-inflammatory and occlusive disorders. Here, we discuss (I) the cellular events involved in the extracellular release of chromatin and NET formation, (II) the devastating consequence of a dysregulated NET formation, and (III) the imbalance between NET formation and clearance. We include the role of NET formation in the occlusion of vessels and ducts, in lung disease, in autoimmune diseases, in chronic oral disorders, in cancer, in the formation of adhesions, and in traumatic spinal cord injury. To develop effective therapies, it is of utmost importance to target pathways that cause decondensation of chromatin during exaggerated NET formation and aggregation. Alternatively, therapies that support the clearance of extracellular chromatin are conceivable.",
author = "Jeeshan Singh and Michael Boettcher and Maximilian D{\"o}lling and Annika Heuer and Bettina Hohberger and Moritz Leppkes and Elisabeth Naschberger and Mirco Schapher and Christine Schauer and Janina Schoen and Michael St{\"u}rzl and Ljubomir Vitkov and Han Wang and Leticija Zlatar and Schett, {Georg A.} and Pisetsky, {David S.} and Ming-Lin Liu and Martin Herrmann and Jasmin Knopf",
year = "2023",
month = apr,
doi = "10.1038/s41418-023-01124-1",
language = "English",
volume = "30",
pages = "861--875",
journal = "CELL DEATH DIFFER",
issn = "1350-9047",
publisher = "NATURE PUBLISHING GROUP",
number = "4",

}

RIS

TY - JOUR

T1 - Moonlighting chromatin: when DNA escapes nuclear control

AU - Singh, Jeeshan

AU - Boettcher, Michael

AU - Dölling, Maximilian

AU - Heuer, Annika

AU - Hohberger, Bettina

AU - Leppkes, Moritz

AU - Naschberger, Elisabeth

AU - Schapher, Mirco

AU - Schauer, Christine

AU - Schoen, Janina

AU - Stürzl, Michael

AU - Vitkov, Ljubomir

AU - Wang, Han

AU - Zlatar, Leticija

AU - Schett, Georg A.

AU - Pisetsky, David S.

AU - Liu, Ming-Lin

AU - Herrmann, Martin

AU - Knopf, Jasmin

PY - 2023/4

Y1 - 2023/4

N2 - Extracellular chromatin, for example in the form of neutrophil extracellular traps (NETs), is an important element that propels the pathological progression of a plethora of diseases. DNA drives the interferon system, serves as autoantigen, and forms the extracellular scaffold for proteins of the innate immune system. An insufficient clearance of extruded chromatin after the release of DNA from the nucleus into the extracellular milieu can perform a secret task of moonlighting in immune-inflammatory and occlusive disorders. Here, we discuss (I) the cellular events involved in the extracellular release of chromatin and NET formation, (II) the devastating consequence of a dysregulated NET formation, and (III) the imbalance between NET formation and clearance. We include the role of NET formation in the occlusion of vessels and ducts, in lung disease, in autoimmune diseases, in chronic oral disorders, in cancer, in the formation of adhesions, and in traumatic spinal cord injury. To develop effective therapies, it is of utmost importance to target pathways that cause decondensation of chromatin during exaggerated NET formation and aggregation. Alternatively, therapies that support the clearance of extracellular chromatin are conceivable.

AB - Extracellular chromatin, for example in the form of neutrophil extracellular traps (NETs), is an important element that propels the pathological progression of a plethora of diseases. DNA drives the interferon system, serves as autoantigen, and forms the extracellular scaffold for proteins of the innate immune system. An insufficient clearance of extruded chromatin after the release of DNA from the nucleus into the extracellular milieu can perform a secret task of moonlighting in immune-inflammatory and occlusive disorders. Here, we discuss (I) the cellular events involved in the extracellular release of chromatin and NET formation, (II) the devastating consequence of a dysregulated NET formation, and (III) the imbalance between NET formation and clearance. We include the role of NET formation in the occlusion of vessels and ducts, in lung disease, in autoimmune diseases, in chronic oral disorders, in cancer, in the formation of adhesions, and in traumatic spinal cord injury. To develop effective therapies, it is of utmost importance to target pathways that cause decondensation of chromatin during exaggerated NET formation and aggregation. Alternatively, therapies that support the clearance of extracellular chromatin are conceivable.

U2 - 10.1038/s41418-023-01124-1

DO - 10.1038/s41418-023-01124-1

M3 - SCORING: Review article

C2 - 36755071

VL - 30

SP - 861

EP - 875

JO - CELL DEATH DIFFER

JF - CELL DEATH DIFFER

SN - 1350-9047

IS - 4

ER -