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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Cyclin-dependent kinase 13

The protein encoded by this gene is a member of the cyclin-dependent serine/threonine protein kinase family. Members of this family are well known for their essential roles as master switches in cell cycle control. The exact function of this protein has not yet been determined, but it may play a role in mRNA processing and may be involved in regulation of hematopoiesis. Alternatively spliced transcript variants have been described.[provided by RefSeq, Dec 2009] (from NCBI)
Top mentioned proteins: SLC4A11, ACID, CAN, CDC2, HAD
Papers on CHED
Autosomal-Dominant Corneal Endothelial Dystrophies CHED1 and PPCD1 Are Allelic Disorders Caused by Non-coding Mutations in the Promoter of OVOL2.
Hardcastle et al., London, United Kingdom. In Am J Hum Genet, Feb 2016
Congenital hereditary endothelial dystrophy 1 (CHED1) and posterior polymorphous corneal dystrophy 1 (PPCD1) are autosomal-dominant corneal endothelial dystrophies that have been genetically mapped to overlapping loci on the short arm of chromosome 20.
[The revised newest IC³D classification of corneal dystrophies].
Weiss et al., New Orleans, United States. In Klin Monbl Augenheilkd, Mar 2015
Congenital hereditary endothelial dystrophy (CHED, formerly CHED2) is an autosomal recessive disorder.
IC3D classification of corneal dystrophies--edition 2.
Lisch et al., New Orleans, United States. In Cornea, Feb 2015
Congenital hereditary endothelial dystrophy (CHED, formerly CHED2) is most likely only an autosomal recessive disorder.
SLC4A11 and the Pathophysiology of Congenital Hereditary Endothelial Dystrophy.
Parker et al., Buffalo, United States. In Biomed Res Int, 2014
Congenital hereditary endothelial dystrophy (CHED) is a rare autosomal recessive disorder of the corneal endothelium characterized by nonprogressive bilateral corneal edema and opacification present at birth.
Fuchs Endothelial Corneal Dystrophy in a Heterozygous Carrier of Congenital Hereditary Endothelial Dystrophy Type 2 with a Novel Mutation in SLC4A11.
Tchah et al., Ch'ŏngju, South Korea. In Ophthalmic Genet, 2014
CHED can be divided into 2 types by the modes of inheritance; CHED type 1 (CHED1) with autosomal dominant inheritance and CHED type 2 (CHED2) with autosomal recessive inheritance.
Interactions among the three adaptation systems of Bacillus subtilis chemotaxis as revealed by an in vitro receptor-kinase assay.
Rao et al., Urbana, United States. In Mol Microbiol, 2014
The Bacillus subtilis chemotaxis pathway employs three systems for sensory adaptation: the methylation system, the CheC/CheD/CheYp system, and the CheV system.
Congenital hereditary endothelial dystrophy caused by SLC4A11 mutations progresses to Harboyan syndrome.
Ali et al., Leeds, United Kingdom. In Cornea, 2014
PURPOSE: Homozygous mutations in SLC4A11 cause 2 rare recessive conditions: congenital hereditary endothelial dystrophy (CHED), affecting the cornea alone, and Harboyan syndrome consisting of corneal dystrophy and sensorineural hearing loss.
Mice with a targeted disruption of Slc4a11 model the progressive corneal changes of congenital hereditary endothelial dystrophy.
Mehta et al., Singapore, Singapore. In Invest Ophthalmol Vis Sci, 2013
PURPOSE: To establish an animal model of congenital hereditary endothelial dystrophy (CHED) using Slc4a11 knockout (KO) mice and evaluate the abnormalities in the cornea and kidney.
Genetics of the corneal endothelial dystrophies: an evidence-based review.
Frausto et al., Los Angeles, United States. In Clin Genet, 2013
In addition, insufficient evidence exists to consider the autosomal dominant form of CHED (CHED1) as distinct from PPCD.
Identification of Host Kinase Genes Required for Influenza Virus Replication and the Regulatory Role of MicroRNAs.
Tripp et al., Athens, United States. In Plos One, 2012
From the screen, 17 HPKs (NPR2, MAP3K1, DYRK3, EPHA6, TPK1, PDK2, EXOSC10, NEK8, PLK4, SGK3, NEK3, PANK4, ITPKB, CDC2L5 (CDK13), CALM2, PKN3, and HK2) were validated as essential for A/WSN/33 influenza virus replication, and 6 HPKs (CDK13, HK2, NEK8, PANK4, PLK4 and SGK3) were identified as vital for both A/WSN/33 and A/New Caledonia/20/99 influenza virus replication.
Identification of novel AR-targeted microRNAs mediating androgen signalling through critical pathways to regulate cell viability in prostate cancer.
Li et al., Shanghai, China. In Plos One, 2012
(3) miR-133b is directly up-regulated by AR, and represses CDC2L5, PTPRK, RB1CC1, and CPNE3, respectively.
Exclusion of positional candidate gene coding region mutations in the common posterior polymorphous corneal dystrophy 1 candidate gene interval.
Papp et al., Los Angeles, United States. In Cornea, 2009
We report the absence of a presumed pathogenic coding region mutation in the common PPCD1 support interval.
The three adaptation systems of Bacillus subtilis chemotaxis.
Ordal et al., Urbana, United States. In Trends Microbiol, 2008
The other two involve CheC, CheD and CheV, which are chemotaxis proteins not found in E. coli.
Congenital hereditary endothelial dystrophy with progressive sensorineural deafness (Harboyan syndrome).
Abramowicz et al., Brussels, Belgium. In Orphanet J Rare Dis, 2007
Autosomal recessive types of CHED (CHED2 and Harboyan syndrome) should carefully be distinguished from the less severe autosomal dominant type CHED1.
CDC2L5, a Cdk-like kinase with RS domain, interacts with the ASF/SF2-associated protein p32 and affects splicing in vivo.
Genevière et al., Saint-Pierre-des-Corps, France. In J Cell Biochem, 2006
Data demonstrate that CDC2L5 is located in the nucleoplasm, where it directly interacts with the ASF/SF2-associated protein p32, a protein involved in splicing regulation.
Mutations in sodium-borate cotransporter SLC4A11 cause recessive congenital hereditary endothelial dystrophy (CHED2).
Aung et al., Singapore, Singapore. In Nat Genet, 2006
Congenital hereditary endothelial dystrophy (CHED) is a heritable, bilateral corneal dystrophy characterized by corneal opacification and nystagmus.
A receptor-modifying deamidase in complex with a signaling phosphatase reveals reciprocal regulation.
Crane et al., Ithaca, United States. In Cell, 2006
The structure of a complex between the signal-terminating phosphatase, CheC, and the receptor-modifying deamidase, CheD, reveals how CheC mimics receptor substrates to inhibit CheD and how CheD stimulates CheC phosphatase activity.
Clinicopathologic correlation and genetic analysis in a case of posterior polymorphous corneal dystrophy.
Richards et al., Ann Arbor, United States. In Am J Ophthalmol, 2003
congenital hereditary endothelial dystrophy 1 (CHED1) and CHED2 loci on chromosome 20 and the collagen, type VIII, alpha-2 (COL8A2) gene were excluded by linkage and haplotype analyses.
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