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@ARTICLE{Rohrer:276867,
author = {L. Rohrer and C. Spohr and C. Beha and R. Griffin and S.
Braun and S. Halbach$^*$ and T. Brummer$^*$},
title = {{A}nalysis of {RAS} and drug induced homo- and
heterodimerization of {RAF} and {KSR}1 proteins in living
cells using split {N}anoluc luciferase.},
journal = {Cell communication and signaling},
volume = {21},
number = {1},
issn = {1478-811X},
address = {London},
publisher = {Biomed Central},
reportid = {DKFZ-2023-01179},
pages = {136},
year = {2023},
abstract = {The dimerization of RAF kinases represents a key event in
their activation cycle and in RAS/ERK pathway activation.
Genetic, biochemical and structural approaches provided key
insights into this process defining RAF signaling output and
the clinical efficacy of RAF inhibitors (RAFi). However,
methods reporting the dynamics of RAF dimerization in living
cells and in real time are still in their infancy. Recently,
split luciferase systems have been developed for the
detection of protein-protein-interactions (PPIs), incl.
proof-of-concept studies demonstrating the
heterodimerization of the BRAF and RAF1 isoforms. Due to
their small size, the Nanoluc luciferase moieties LgBiT and
SmBiT, which reconstitute a light emitting holoenzyme upon
fusion partner promoted interaction, appear as well-suited
to study RAF dimerization. Here, we provide an extensive
analysis of the suitability of the Nanoluc system to study
the homo- and heterodimerization of BRAF, RAF1 and the
related KSR1 pseudokinase. We show that KRASG12V promotes
the homo- and heterodimerization of BRAF, while considerable
KSR1 homo- and KSR1/BRAF heterodimerization already occurs
in the absence of this active GTPase and requires a salt
bridge between the CC-SAM domain of KSR1 and the
BRAF-specific region. We demonstrate that loss-of-function
mutations impairing key steps of the RAF activation cycle
can be used as calibrators to gauge the dynamics of
heterodimerization. This approach identified the RAS-binding
domains and the C-terminal 14-3-3 binding motifs as
particularly critical for the reconstitution of RAF mediated
LgBiT/SmBiT reconstitution, while the dimer interface was
less important for dimerization but essential for downstream
signaling. We show for the first time that BRAFV600E, the
most common BRAF oncoprotein whose dimerization status is
controversially portrayed in the literature, forms
homodimers in living cells more efficiently than its
wildtype counterpart. Of note, Nanoluc activity
reconstituted by BRAFV600E homodimers is highly sensitive to
the paradox-breaking RAFi PLX8394, indicating a dynamic and
specific PPI. We report the effects of eleven ERK pathway
inhibitors on RAF dimerization, incl. third-generation
compounds that are less-defined in terms of their dimer
promoting abilities. We identify Naporafenib as a potent and
long-lasting dimerizer and show that the split Nanoluc
approach discriminates between type I, I1/2 and II RAFi.
Video Abstract.},
keywords = {BRAF (Other) / Belvarafenib (Other) / KRAS (Other) / KSR1
(Other) / LgBiT (Other) / MAPK pathway (Other) / NanoBit
Oplophorus luciferase (Other) / RAF1 (Other) / SmBiT (Other)
/ Sorafenib (Other)},
cin = {FR01},
ddc = {570},
cid = {I:(DE-He78)FR01-20160331},
pnm = {899 - ohne Topic (POF4-899)},
pid = {G:(DE-HGF)POF4-899},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:37316874},
doi = {10.1186/s12964-023-01146-9},
url = {https://inrepo02.dkfz.de/record/276867},
}