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onsdag 23 oktober 2019

KLHL22 (22q11.21), KELCHL, paikantaa mitoosissa PKL1-polokinaasin

https://www.ncbi.nlm.nih.gov/gene/84861
Also known as KELCHL
Expression Ubiquitous expression in brain (RPKM 3.8), thyroid (RPKM 3.7) and 25 other tissues See more Orthologs mouse all
 
Conserved Domains (2) summary
sd00038
Location:340385
Kelch; KELCH repeat [structural motif]
cl28614
Location:52592
BTB; Broad-Complex, Tramtrack and Bric a brac

https://www.ncbi.nlm.nih.gov/pubmed/23455478

2013 Apr;15(4):430-9. doi: 10.1038/ncb2695. Epub 2013 Mar 3.
Ubiquitylation-dependent localization of PLK1 in mitosis.
Beck J1, Maerki S, Posch M, Metzger T, Persaud A, Scheel H, Hofmann K, Rotin D, Pedrioli P, Swedlow JR, Peter M, Sumara I.Institute of Biochemistry, ETH Zurich, Schafmattstrasse 18, 8093 Zurich, Switzerland. Abstract
Polo-like kinase 1 (PLK1) critically regulates mitosis through its dynamic localization to kinetochores, centrosomes and the midzone. The polo-box domain (PBD) and activity of PLK1 mediate its recruitment to mitotic structures, but the mechanisms regulating PLK1 dynamics remain poorly understood.
Here, we identify PLK1 as a target of the cullin 3 (CUL3)-based E3 ubiquitin ligase, containing the BTB adaptor KLHL22, which regulates chromosome alignment and PLK1 kinetochore localization but not PLK1 stability. In the absence of KLHL22, PLK1 accumulates on kinetochores, resulting in activation of the spindle assembly checkpoint (SAC).
 CUL3-KLHL22 ubiquitylates Lys 492, located within the PBD, leading to PLK1 dissociation from kinetochore phosphoreceptors. Expression of a non-ubiquitylatable PLK1-K492R mutant phenocopies inactivation of CUL3-KLHL22.
KLHL22 associates with the mitotic spindle and its interaction with PLK1 increases on chromosome bi-orientation. Our data suggest that CUL3-KLHL22-mediated ubiquitylation signals degradation-independent removal of PLK1 from kinetochores and SAC satisfaction, which are required for faithful mitosis.

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