Zobrazeno 1 - 3
of 3
pro vyhledávání: '"Susanne R Bruekner"'
Autor:
Susanne R Bruekner, Wietske Pieters, Alexander Fish, A Manuel Liaci, Serge Scheffers, Emily Rayner, Daphne Kaldenbach, Lisa Drost, Marleen Dekker, Sandrine van Hees-Stuivenberg, Elly Delzenne-Goette, Charlotte de Konink, Hellen Houlleberghs, Hendrikus Jan Dubbink, Abeer AlSaegh, Niels de Wind, Friedrich Förster, Hein te Riele, Titia K Sixma
Publikováno v:
Nucleic Acids Research, 51(3), 1173-1188. Oxford University Press
Bruekner, S R, Pieters, W, Fish, A, Liaci, A M, Scheffers, S, Rayner, E, Kaldenbach, D, Drost, L, Dekker, M, van Hees-Stuivenberg, S, Delzenne-Goette, E, de Konink, C, Houlleberghs, H, Dubbink, H J, Alsaegh, A, de Wind, N, Förster, F, te Riele, H & Sixma, T K 2023, ' Unexpected moves : a conformational change in MutSα enables high-affinity DNA mismatch binding ', Nucleic Acids Research, vol. 51, no. 3, pp. 1173-1188 . https://doi.org/10.1093/nar/gkad015
Bruekner, S R, Pieters, W, Fish, A, Liaci, A M, Scheffers, S, Rayner, E, Kaldenbach, D, Drost, L, Dekker, M, van Hees-Stuivenberg, S, Delzenne-Goette, E, de Konink, C, Houlleberghs, H, Dubbink, H J, Alsaegh, A, de Wind, N, Förster, F, te Riele, H & Sixma, T K 2023, ' Unexpected moves : a conformational change in MutSα enables high-affinity DNA mismatch binding ', Nucleic Acids Research, vol. 51, no. 3, pp. 1173-1188 . https://doi.org/10.1093/nar/gkad015
The DNA mismatch repair protein MutSα recognizes wrongly incorporated DNA bases and initiates their correction during DNA replication. Dysfunctions in mismatch repair lead to a predisposition to cancer. Here, we study the homozygous mutation V63E in
Autor:
Lars Kullmann, Fabian A. Renschler, Christine Henzler, Paulin Salomon, Amrita Mukherjee, Mira C. Schütz-Stoffregen, Susanne R. Bruekner, Michael P. Krahn, Silke Wiesner, Tony Pawson
Publikováno v:
Science Signaling. 11
Polarity is a fundamental property of most cell types. The Par protein complex is a major driving force in generating asymmetrically localized protein networks and consists of atypical protein kinase C (aPKC), Par3, and Par6. Dysfunction of this comp
Autor:
Joseph T. Opferman, Michelle Stewart, Loren D. Walensky, Evripidis Gavathiotis, Nicole A. Cohen, Brian Koss, Jared L. Tepper, Susanne R. Bruekner
Publikováno v:
Chemistrybiology. 19(9)
SummaryCancer cells hijack BCL-2 family survival proteins to suppress the death effectors and thereby enforce an immortal state. This is accomplished biochemically by an antiapoptotic surface groove that neutralizes the proapoptotic BH3 α helix of d