Structural Basis of BRCC36 Function in DNA Repair and Immune Regulation

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Structural Basis of BRCC36 Function in DNA Repair and Immune Regulation. / Rabl, Julius; Bunker, Richard D; Schenk, Andreas D; Cavadini, Simone; Gill, Mark E; Abdulrahman, Wassim; Andrés-Pons, Amparo; Luijsterburg, Martijn S; Ibrahim, Adel F M; Branigan, Emma; Aguirre, Jacob D; Marceau, Aimee H; Guérillon, Claire; Bouwmeester, Tewis; Hassiepen, Ulrich; Peters, Antoine H F M; Renatus, Martin; Gelman, Laurent; Rubin, Seth M; Mailand, Niels; van Attikum, Haico; Hay, Ronald T.; Thomä, Nicolas H.

In: Molecular Cell, Vol. 75, No. 3, 2019, p. 483-497.e9.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Rabl, J, Bunker, RD, Schenk, AD, Cavadini, S, Gill, ME, Abdulrahman, W, Andrés-Pons, A, Luijsterburg, MS, Ibrahim, AFM, Branigan, E, Aguirre, JD, Marceau, AH, Guérillon, C, Bouwmeester, T, Hassiepen, U, Peters, AHFM, Renatus, M, Gelman, L, Rubin, SM, Mailand, N, van Attikum, H, Hay, RT & Thomä, NH 2019, 'Structural Basis of BRCC36 Function in DNA Repair and Immune Regulation', Molecular Cell, vol. 75, no. 3, pp. 483-497.e9. https://doi.org/10.1016/j.molcel.2019.06.002

APA

Rabl, J., Bunker, R. D., Schenk, A. D., Cavadini, S., Gill, M. E., Abdulrahman, W., Andrés-Pons, A., Luijsterburg, M. S., Ibrahim, A. F. M., Branigan, E., Aguirre, J. D., Marceau, A. H., Guérillon, C., Bouwmeester, T., Hassiepen, U., Peters, A. H. F. M., Renatus, M., Gelman, L., Rubin, S. M., ... Thomä, N. H. (2019). Structural Basis of BRCC36 Function in DNA Repair and Immune Regulation. Molecular Cell, 75(3), 483-497.e9. https://doi.org/10.1016/j.molcel.2019.06.002

Vancouver

Rabl J, Bunker RD, Schenk AD, Cavadini S, Gill ME, Abdulrahman W et al. Structural Basis of BRCC36 Function in DNA Repair and Immune Regulation. Molecular Cell. 2019;75(3):483-497.e9. https://doi.org/10.1016/j.molcel.2019.06.002

Author

Rabl, Julius ; Bunker, Richard D ; Schenk, Andreas D ; Cavadini, Simone ; Gill, Mark E ; Abdulrahman, Wassim ; Andrés-Pons, Amparo ; Luijsterburg, Martijn S ; Ibrahim, Adel F M ; Branigan, Emma ; Aguirre, Jacob D ; Marceau, Aimee H ; Guérillon, Claire ; Bouwmeester, Tewis ; Hassiepen, Ulrich ; Peters, Antoine H F M ; Renatus, Martin ; Gelman, Laurent ; Rubin, Seth M ; Mailand, Niels ; van Attikum, Haico ; Hay, Ronald T. ; Thomä, Nicolas H. / Structural Basis of BRCC36 Function in DNA Repair and Immune Regulation. In: Molecular Cell. 2019 ; Vol. 75, No. 3. pp. 483-497.e9.

Bibtex

@article{a05cec5443a44e2ca60668cd6ff997af,
title = "Structural Basis of BRCC36 Function in DNA Repair and Immune Regulation",
abstract = "In mammals, ∼100 deubiquitinases act on ∼20,000 intracellular ubiquitination sites. Deubiquitinases are commonly regarded as constitutively active, with limited regulatory and targeting capacity. The BRCA1-A and BRISC complexes serve in DNA double-strand break repair and immune signaling and contain the lysine-63 linkage-specific BRCC36 subunit that is functionalized by scaffold subunits ABRAXAS and ABRO1, respectively. The molecular basis underlying BRCA1-A and BRISC function is currently unknown. Here we show that in the BRCA1-A complex structure, ABRAXAS integrates the DNA repair protein RAP80 and provides a high-affinity binding site that sequesters the tumor suppressor BRCA1 away from the break site. In the BRISC structure, ABRO1 binds SHMT2α, a metabolic enzyme enabling cancer growth in hypoxic environments, which we find prevents BRCC36 from binding and cleaving ubiquitin chains. Our work explains modularity in the BRCC36 DUB family, with different adaptor subunits conferring diversified targeting and regulatory functions.",
author = "Julius Rabl and Bunker, {Richard D} and Schenk, {Andreas D} and Simone Cavadini and Gill, {Mark E} and Wassim Abdulrahman and Amparo Andr{\'e}s-Pons and Luijsterburg, {Martijn S} and Ibrahim, {Adel F M} and Emma Branigan and Aguirre, {Jacob D} and Marceau, {Aimee H} and Claire Gu{\'e}rillon and Tewis Bouwmeester and Ulrich Hassiepen and Peters, {Antoine H F M} and Martin Renatus and Laurent Gelman and Rubin, {Seth M} and Niels Mailand and {van Attikum}, Haico and Hay, {Ronald T.} and Thom{\"a}, {Nicolas H}",
year = "2019",
doi = "10.1016/j.molcel.2019.06.002",
language = "English",
volume = "75",
pages = "483--497.e9",
journal = "Molecular Cell",
issn = "1097-2765",
publisher = "Cell Press",
number = "3",

}

RIS

TY - JOUR

T1 - Structural Basis of BRCC36 Function in DNA Repair and Immune Regulation

AU - Rabl, Julius

AU - Bunker, Richard D

AU - Schenk, Andreas D

AU - Cavadini, Simone

AU - Gill, Mark E

AU - Abdulrahman, Wassim

AU - Andrés-Pons, Amparo

AU - Luijsterburg, Martijn S

AU - Ibrahim, Adel F M

AU - Branigan, Emma

AU - Aguirre, Jacob D

AU - Marceau, Aimee H

AU - Guérillon, Claire

AU - Bouwmeester, Tewis

AU - Hassiepen, Ulrich

AU - Peters, Antoine H F M

AU - Renatus, Martin

AU - Gelman, Laurent

AU - Rubin, Seth M

AU - Mailand, Niels

AU - van Attikum, Haico

AU - Hay, Ronald T.

AU - Thomä, Nicolas H

PY - 2019

Y1 - 2019

N2 - In mammals, ∼100 deubiquitinases act on ∼20,000 intracellular ubiquitination sites. Deubiquitinases are commonly regarded as constitutively active, with limited regulatory and targeting capacity. The BRCA1-A and BRISC complexes serve in DNA double-strand break repair and immune signaling and contain the lysine-63 linkage-specific BRCC36 subunit that is functionalized by scaffold subunits ABRAXAS and ABRO1, respectively. The molecular basis underlying BRCA1-A and BRISC function is currently unknown. Here we show that in the BRCA1-A complex structure, ABRAXAS integrates the DNA repair protein RAP80 and provides a high-affinity binding site that sequesters the tumor suppressor BRCA1 away from the break site. In the BRISC structure, ABRO1 binds SHMT2α, a metabolic enzyme enabling cancer growth in hypoxic environments, which we find prevents BRCC36 from binding and cleaving ubiquitin chains. Our work explains modularity in the BRCC36 DUB family, with different adaptor subunits conferring diversified targeting and regulatory functions.

AB - In mammals, ∼100 deubiquitinases act on ∼20,000 intracellular ubiquitination sites. Deubiquitinases are commonly regarded as constitutively active, with limited regulatory and targeting capacity. The BRCA1-A and BRISC complexes serve in DNA double-strand break repair and immune signaling and contain the lysine-63 linkage-specific BRCC36 subunit that is functionalized by scaffold subunits ABRAXAS and ABRO1, respectively. The molecular basis underlying BRCA1-A and BRISC function is currently unknown. Here we show that in the BRCA1-A complex structure, ABRAXAS integrates the DNA repair protein RAP80 and provides a high-affinity binding site that sequesters the tumor suppressor BRCA1 away from the break site. In the BRISC structure, ABRO1 binds SHMT2α, a metabolic enzyme enabling cancer growth in hypoxic environments, which we find prevents BRCC36 from binding and cleaving ubiquitin chains. Our work explains modularity in the BRCC36 DUB family, with different adaptor subunits conferring diversified targeting and regulatory functions.

U2 - 10.1016/j.molcel.2019.06.002

DO - 10.1016/j.molcel.2019.06.002

M3 - Journal article

C2 - 31253574

VL - 75

SP - 483-497.e9

JO - Molecular Cell

JF - Molecular Cell

SN - 1097-2765

IS - 3

ER -

ID: 227087306