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LIM Domain Kinase 1 (LIMK1), Human Kinase Domain; A Target Enabling Package

Documentation:
A description of the materials and methods is included within the TEP datasheet. Loss of the translational repressor FMRP in fragile X syndrome causes upregulation of the type II BMP receptor BMPR2 and its non-canonical signalling via the kinase LIMK1. LIMK1 performs inhibitory phosphorylation on cofilin proteins blocking their actin-severing activity. Excessive BMPR2-LIMK1 activation was associated with dendritic spine and behavioural defects in animal models that could be rescued by BMPR2 knockdown or LIMK1 inhibition. Here we present a target enabling package for the therapeutic target LIMK1. We include crystal structures of BMPR2, LIMK1, LIMK2 and the LIMK1-cofilin complex, as well as multiple assays for small molecule inhibitor screening. Finally, we identify a series of allosteric LIMK1 inhibitors with promising potency and selectivity that may potentially allow the development of a safe drug for this chronic indication.
Version:
3

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Authors/Creators


More by this author/creator
Institution:
University of Oxford
Division:
MSD
Department:
NDM
Sub department:
Structural Genomics Consortium
Role:
Principal Investigator (PI), Creator
ORCID:
0000-0001-6757-0436

Contributors

Institution:
University of Oxford
Division:
MSD
Department:
NDM
Role:
Researcher
Institution:
University of Oxford
Division:
MPLS
Department:
Chemistry
Sub department:
Organic Chemistry
Role:
Researcher
ORCID:
0000-0001-7552-4966
Institution:
University of Oxford
Division:
MSD
Department:
NDM
Sub department:
Structural Genomics Consortium
Role:
Researcher
Institution:
University of Oxford
Division:
MSD
Department:
NDM
Sub department:
Structural Genomics Consortium
Role:
Researcher
Institution:
University of Oxford
Division:
MSD
Department:
NDM
Sub department:
Structural Genomics Consortium
Role:
Researcher


More from this funder
Funder identifier:
https://ror.org/029chgv08
Grant:
106169/ZZ14/Z


Publisher:
University of Oxford
Publication date:
2018
Version number:
3

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