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Articles by X Kong
Total Records ( 4 ) for X Kong
  N. L Smith , M. H Chen , A Dehghan , D. P Strachan , S Basu , N Soranzo , C Hayward , I Rudan , M Sabater Lleal , J. C Bis , M. P. M de Maat , A Rumley , X Kong , Q Yang , F. M. K Williams , V Vitart , H Campbell , A Malarstig , K. L Wiggins , C. M Van Duijn , W. L McArdle , J. S Pankow , A. D Johnson , A Silveira , B McKnight , A. G Uitterlinden , Aleksic Wellcome Trust Case Control Consortium; , J. B Meigs , A Peters , W Koenig , M Cushman , S Kathiresan , J. I Rotter , E. G Bovill , A Hofman , E Boerwinkle , G. H Tofler , J. F Peden , B. M Psaty , F Leebeek , A. R Folsom , M. G Larson , T. D Spector , A. F Wright , J. F Wilson , A Hamsten , T Lumley , J. C. M Witteman , W Tang and C. J. O'Donnell

Background— Plasma levels of coagulation factors VII (FVII), VIII (FVIII), and von Willebrand factor (vWF) influence risk of hemorrhage and thrombosis. We conducted genome-wide association studies to identify new loci associated with plasma levels.

Methods and Results— The setting of the study included 5 community-based studies for discovery comprising 23 608 European-ancestry participants: Atherosclerosis Risk In Communities Study, Cardiovascular Health Study, British 1958 Birth Cohort, Framingham Heart Study, and Rotterdam Study. All subjects had genome-wide single-nucleotide polymorphism (SNP) scans and at least 1 phenotype measured: FVII activity/antigen, FVIII activity, and vWF antigen. Each study used its genotype data to impute to HapMap SNPs and independently conducted association analyses of hemostasis measures using an additive genetic model. Study findings were combined by meta-analysis. Replication was conducted in 7604 participants not in the discovery cohort. For FVII, 305 SNPs exceeded the genome-wide significance threshold of 5.0x10–8 and comprised 5 loci on 5 chromosomes: 2p23 (smallest P value 6.2x10–24), 4q25 (3.6x10–12), 11q12 (2.0x10–10), 13q34 (9.0x10–259), and 20q11.2 (5.7x10–37). Loci were within or near genes, including 4 new candidate genes and F7 (13q34). For vWF, 400 SNPs exceeded the threshold and marked 8 loci on 6 chromosomes: 6q24 (1.2x10–22), 8p21 (1.3x10–16), 9q34 (<5.0x10–324), 12p13 (1.7x10–32), 12q23 (7.3x10–10), 12q24.3 (3.8x10–11), 14q32 (2.3x10–10), and 19p13.2 (1.3x10–9). All loci were within genes, including 6 new candidate genes, as well as ABO (9q34) and VWF (12p13). For FVIII, 5 loci were identified and overlapped vWF findings. Nine of the 10 new findings were replicated.

Conclusions— New genetic associations were discovered outside previously known biological pathways and may point to novel prevention and treatment targets of hemostasis disorders.

  T Yusufzai , X Kong , K Yokomori and J. T. Kadonaga

HepA-related protein (HARP) (also known as SMARCAL1) is an ATP-driven annealing helicase that catalyzes the formation of dsDNA from complementary Replication protein A (RPA)-bound ssDNA. Here we find that HARP contains a conserved N-terminal motif that is necessary and sufficient for binding to RPA. This RPA-binding motif is not required for annealing helicase activity, but is essential for the recruitment of HARP to sites of laser-induced DNA damage. These findings suggest that the interaction of HARP with RPA increases the concentration of annealing helicase activity in the vicinity of ssDNA regions to facilitate processes such as DNA repair.

  S Wu , W Wang , X Kong , L. M Congdon , K Yokomori , M. W Kirschner and J. C. Rice

Although the PR-Set7/Set8/KMT5a histone H4 Lys 20 monomethyltransferase (H4K20me1) plays an essential role in mammalian cell cycle progression, especially during G2/M, it remained unknown how PR-Set7 itself was regulated. In this study, we discovered the mechanisms that govern the dynamic regulation of PR-Set7 during mitosis, and that perturbation of these pathways results in defective mitotic progression. First, we found that PR-Set7 is phosphorylated at Ser 29 (S29) specifically by the cyclin-dependent kinase 1 (cdk1)/cyclinB complex, primarily from prophase through early anaphase, subsequent to global accumulation of H4K20me1. While S29 phosphorylation did not affect PR-Set7 methyltransferase activity, this event resulted in the removal of PR-Set7 from mitotic chromosomes. S29 phosphorylation also functions to stabilize PR-Set7 by directly inhibiting its interaction with the anaphase-promoting complex (APC), an E3 ubiquitin ligase. The dephosphorylation of S29 during late mitosis by the Cdc14 phosphatases was required for APCcdh1-mediated ubiquitination of PR-Set7 and subsequent proteolysis. This event is important for proper mitotic progression, as constitutive phosphorylation of PR-Set7 resulted in a substantial delay between metaphase and anaphase. Collectively, we elucidated the molecular mechanisms that control PR-Set7 protein levels during mitosis, and demonstrated that its orchestrated regulation is important for normal mitotic progression.

  X Kong , H Gan , Y Hao , C Cheng , J Jiang , Y Hong , J Yang , H Zhu , Y Chi , X Yun and J. Gu

CDK11p58, a CDK11 family Ser/Thr kinase, is a G2/M specific protein and contributed to regulation of cell cycle, transcription and apoptotic signal transduction. Recently, CDK11p58 has been reported to exert important functions in mitotic process, such as the regulation of bipolar spindle formation and sister chromatid cohesion. Here, we identified p21 activated kinase 1 (PAK1) as a new CDK11p58 substrate and we mapped a new phosphorylation site of Ser174 on PAK1. By mutagenesis, we created PAK1174A and PAK1174E, which mimic the dephosphorylated and phosphorylated form of PAK1; further analysis showed PAK1174E could be recruited to myosin V motor complex through binding to dynein light chain 2 (DLC2). PAK1174E could accelerate the mitosis progression in a nocodazole blocked cell model, while PAK1174A exhibited an opposite role. Our results indicated PAK1 may serve as a downstream effector of CDK11p58 during mitosis progression.

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