Yun-qiang Liu

State Key Laboratory of Biotherapy

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Ying Shen

Chinese Academy of Sciences

Yi-lu Lu

State Key Laboratory of Biotherapy

Yongyi Ma

Nantong University

Lei Li

Sichuan University

Wang Xiang-wen

Hengyang Normal University

Rui Xue

Zhongshan Hospital

Songyu Yu

Shanghai Jiao Tong University

Yufeng Tang

Mianyang Central Hospital

Dachang Tao

State Key Laboratory of Biotherapy

Lili Zhao

Shandong Agricultural University

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Sichuan University

State Key Laboratory of Biotherapy

West China Hospital of Sichuan University

West China Medical Center of Sichuan University

University of Chinese Academy of Sciences

Tongji University

Shanghai Jiao Tong University

Fudan University

Northwest A&F University

Chongqing Medical University

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[Clinical characteristics and spastin gene mutation analysis on an autosomal dominant kindred with hereditary spastic paraplegia].

Zhonghua yixue yichuanxue zazhi (2007)

Ling Liu Yun-qiang Liu Yanming Xu Rui Xue Yufeng Tang

To investigate the clinical characteristics and analyze spastin gene mutation on a kindred with hereditary spastic paraplegia (HSP).All family members were studied through clinical examinations. The proband and another two patients in this kindred were subjected to electromyography (EMG) examinations. The proband was subjected to thoracic MRI examination too. Mutation analysis of spastin gene was screened by polymerase chain reaction combined with DNA sequencing in the proband and his father.All patients in the kindred manifested as classical HSP. Thoracic MRI revealed atrophies of the spinal cord in the proband. No abnormal spastin gene mutation was detected in these two patients.This kindred has typical clinical manifestations of HSP. The pathogenesis has no association with mutation of the exons of spastin gene.

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Hereditary Spastic Paraplegia

Paraplegia

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Common AZFc structure may possess the optimal spermatogenesis efficiency relative to the rearranged structures mediated by non-allele homologous recombination

Scientific Reports (2015)

Bo Yang Yongyi Ma Yun-qiang Liu Lei Li Dong Yang

Abstract The azoopsermia factor c (AZFc) region of human Y-chromosome is an essential genomic segment for spermatogenesis with frequent non-allele homologous recombination (NAHR). Recent case-control studies on the association of the NAHR-based AZFc structural mutations with spermatogenic failure produced inconsistent results. To more precisely evaluate their spermatogenesis effects, we investigated the correlation between the subdivided AZFc mutations and sperm production in 3,439 Han Chinese males. Our results showed that both partial AZFc deletion-only and primary duplication mutation presented a significant risk for decreased sperm production. Restoration of the reduced dosage of the AZFc content to the normal level had a milder effect, whereas an overdose of the AZFc content arising from multiple duplications of a partial AZFc-deleted structure produced a more serious consequence compared to the partial deletion-only mutation. Additionally, the AZFc-mutated structures with excessive NAHR-substrate showed a notably negative effect on spermatogenesis. These results suggest that the recurrent NAHR-based AZFc mutations may be associated with decreased spermatogenesis efficiency in present population. More significantly, our finding implies that the overdose of AZFc NAHR-substrate may produce an additional risk for the massive AZFbc deletions during the multi-stage division process of germ cells and thus impair the global spermatogenesis efficiency in the carriers.

Non-allelic homologous recombination

10.1038/srep10551

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Segment-based traffic smoothing algorithm for VBR video stream

Journal of Zhejiang University. Science A (2006)

Yun-qiang Liu Songyu Yu Wang Xiang-wen Jun Zhou

Burstiness

Smoothing

10.1631/jzus.2006.a0543

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CLOCK and BMAL1 stabilize and activate RHOA to promote F-actin formation in cancer cells

Experimental & Molecular Medicine (2018)

Tengjiao Ma Zhiwei Zhang Yi-lu Lu Yingying Zhang Dachang Tao

Circadian genes control most of the physiological functions in cancer cells, including cell proliferation, migration, and invasion. The CLOCK and BMAL1 complex plays a central role in circadian rhythms. Previous studies have shown that circadian genes may act as oncogenes or tumor-suppressor genes. In addition, F-actin, regulated by RHOA, has been shown to participate in tumor progression. However, the roles of the CLOCK and BMAL1 genes in the regulation of tumor progression via the RHOA-ROCK-CFL pathway remain largely unclear. Here we first indicate that the rearrangement of F-actin is regulated by CLOCK and BMAL1. We found that CLOCK and BMAL1 can upregulate RHOA expression by inhibiting CUL3-mediated ubiquitination and activate RHOA by reducing the interaction between RHOA and RhoGDI. Consequently, CLOCK and BMAL1 control the expression of the components of the RHOA-ROCK-CFL pathway, which alters the dynamics of F-actin/G-actin turnover and promotes cancer cell proliferation, migration, and invasion. In conclusion, our research proposes a novel insight into the role of CLOCK and BMAL1 in tumor cells.

10.1038/s12276-018-0156-4

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Citations (46)