Tao Liu

Chongqing Medical University

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

Xingye Xu

Chinese Academy of Medical Sciences & Peking Union Medical College

Haiping Que

Institute of Basic Medical Sciences of the Chinese Academy of Medical Sciences

Shaojun Liu

Second Affiliated Hospital of Guangzhou Medical University

Zhenlian Ma

Institute of Basic Medical Sciences of the Chinese Academy of Medical Sciences

Qi Jin

Chinese Academy of Medical Sciences & Peking Union Medical College

Wuju Li

Academy of Military Medical Sciences

Shuqian Jing

Institute of Basic Medical Sciences of the Chinese Academy of Medical Sciences

Lihong Chen

Fujian Medical University

Jian Yang

Chinese Academy of Medical Sciences & Peking Union Medical College

Lan Huang

University of California, Irvine

Cooperative Institutions

Chinese Academy of Sciences

Academy of Military Medical Sciences

Chinese Academy of Medical Sciences & Peking Union Medical College

Fudan University

Chongqing Medical University

Peking University

Central South University

Huazhong University of Science and Technology

Chinese Academy of Agricultural Sciences

Zhejiang University

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

Identification of sequence variants associated with severe microtia-astresia by targeted sequencing

BMC Medical Genomics (2019)

Pu Wang Yibei Wang Xinmiao Fan Yaping Liu Yue Fan

Microtia-atresia is characterized by abnormalities of the auricle (microtia) and aplasia or hypoplasia of the external auditory canal, often associated with middle ear abnormalities. To date, no causal genetic mutations or genes have been identified in microtia-atresia patients. We designed a panel of 131 genes associated with external/middle or inner ear deformity. Targeted genomic capturing combined with next-generation sequencing (NGS) was utilized to screen for mutations in 40 severe microtia-atresia patients. Mutations detected by NGS were filtered and validated. And then mutations were divided into three categories—rare or novel variants, low-frequency variants and common variants—based on their frequency in the public database. The rare or novel mutations were prioritized by pathogenicity analysis. For the low-frequency variants and common variants, we used association studies to explore risk factors of severe microtia-atresia. Sixty-five rare heterozygous mutations of 42 genes were identified in 27 (67.5%) severe microtia-atresia patients. Association studies to determine genes that were potentially pathogenic found that PLEC, USH2A, FREM2, DCHS1, GLI3, POMT1 and GBA genes were significantly associated with severe microtia-atresia. Of these, DCHS1 was strongly suggested to cause severe microtia-atresia as it was identified by both low-frequency and common variants association studies. A rare mutation (c.481C > T, p.R161C) in DCHS1 identified in one individual may be deleterious and may cause severe microtia-atresia. We identified several genes that were significantly associated with severe microtia-atresia. The findings provide new insights into genetic background of external ear deformities.

Microtia

10.1186/s12920-019-0475-x

Cite

Citations (18)

Different Effects of p52SHC1 and p52SHC3 on the Cell Cycle of Neurons and Neural Stem Cells

Journal of Cellular Physiology (2015)

Ning Tang Dan Lyu Tao Liu Fangjin Chen Shuqian Jing

SHC3 is exclusively expressed in postmitotic neurons, while SHC1 is found in neural stem cells and neural precursor cells but absent in mature neurons. In this study, we discovered that suppression of p52SHC1 expression by RNA interference resulted in proliferation defects in neural stem cells, along with significantly reduced protein levels of cyclin E and cyclin A. At the same time, p52SHC3 RNAi caused cell cycle re-entry (9.54% in S phase and 5.70% in G2-M phase) in primary neurons with significantly up-regulated expression of cyclin D1, cyclin E, cyclin A, CDK2, and phosphorylated CDK2. When p52SHC3 was overexpressed, the cell cycle of neural stem cells was arrested with reduced protein levels of cyclin D1, cyclin E, and cyclin A, while overexpression of p52SHC1 did not result in significant changes in postmitotic neurons. Our results indicate that p52SHC3 plays an important role in maintaining the mitotic quiescence of neurons, while p52SHC1 regulates the proliferation of neural stem cells.

Cyclin A

Cyclin E

Cyclin B1

Cyclin A2

Cyclin D

Cyclin B

Cyclin E1

10.1002/jcp.25069

Cite

Citations (3)

Portable, intelligent MIECL sensing platform for ciprofloxacin detection using a fast convolutional neural networks-assisted Tb@Lu2O3 nanoemitter

Food Chemistry (2024)

Zhiwei Lu Yonghui Gong Chengao Shen Hao Chen Weiling Zhu

10.1016/j.foodchem.2024.138656

Cite

Citations (11)

Generation of New Landomycins by Combinatorial Biosynthetic Manipulation of the LndGT4 Gene of the Landomycin E Cluster in S. globisporus

Chemistry & Biology (2004)

Bohdan Ostash Uwe Rix Lily Rix Tao Liu Felipe Lombó

Gene cluster

10.1016/j.chembiol.2004.03.011

Cite

Citations (64)

Portable, Intelligent Miecl Sensing Platform for Ciprofloxacin Detection Using a Fast Convolutional Neural Networks-Assisted Tb@Lu2o3 Nanoemitter

Zhiwei Lu Yonghui Gong Chengao Shen Hao Chen Weiling Zhu

Environmental pollution caused by ciprofloxacin is a major problem of global public health. A machine learning-assisted portable smartphone-based visualized molecularly imprinted electrochemiluminescence (MIECL) sensor was developed for the highly selective and sensitive detection of ciprofloxacin (CFX) in food. To boost the efficiency of electrochemiluminescence (ECL), oxygen vacancies (OVs) enrichment was introduced into the flower-like Tb@Lu2O3nanoemitter. With the specific recognition reaction between MIP as capture probes and CFX as detection target, ECL signal significantly decreased. According to, CFX analysis was determined by traditional ECL analyzer detector in the concentration range from 5×10-4 to 5×102 μmol L-1 with the detection limit (LOD) of 0.095 nmol L-1 (S/N=3). Analysis of luminescence images using fast electrochemiluminescence judgment network (FEJ-Net) models, achieving portable and intelligent quickly analysis of CFX. The proposed MIECL sensor was used for CFX analysis in real meat samples and satisfactory results, as well as efficient selectivity and good stability.

10.2139/ssrn.4662974

Cite

Citations (1)

[Expression of ERK1/2 MAPK signaling transduction pathway in esophageal cancers in Kazakh patients].

Zhonghua zhongliu zazhi (2011)

Shutao Zheng Tao Liu Aerziguli Middottuersun Qi Huo Qing Liu

Source

Cite

Citations (6)

Heat shock protein 90β stabilizes focal adhesion kinase and enhances cell migration and invasion in breast cancer cells

Experimental Cell Research (2014)

Xiangyang Xiong Yao Wang Chengmei Liu Quqin Lu Tao Liu

10.1016/j.yexcr.2014.05.018

Cite

Citations (25)

Cytotoxic cis-ruthenium(iii) bis(amidine) complexes

Dalton Transactions (2023)

Tao Liu Pan Chen Hua‐Tian Shi Tao Huang Yong‐Liang Huang

In chemotherapy, the search for ruthenium compounds as alternatives to platinum compounds is proposed because of their unique properties. However, the geometry effect of ruthenium complexes is sparely investigated. In this paper, we report the synthesis of a series of bis(acetylacetonato)ruthenium(III) complexes bearing two amidines (1-) in a cis configuration. These complexes are highly cytotoxic against various cancer cell lines, including a cisplatin-resistant cell line. In vitro studies suggested that the representative complex can induce cell cycle G0/G1 phase arrest, decrease the mitochondrial membrane potential, elevate the intracellular reactive oxygen species level, and cause DNA damage and caspase-mediated mitochondrial pathway apoptosis in NCI-H460 cells. In vivo, it can effectively inhibit tumor xenograft growth in nude mouse models with no body weight loss. In combination with the reported trans-bis(amidine)ruthenium(III) complexes, we found that ruthenium(III) bis(amidine) complexes could be cytotoxic in both trans and cis geometries, which is in contrast to platinum-based compounds.

Amidine

10.1039/d3dt00328k

Cite

Citations (4)

Comparison of Immunological Responses of Plague Vaccines F1 + rV270 and EV76 in Chinese-Origin Rhesus Macaque, Macaca mulatta

Scandinavian Journal of Immunology (2010)

Yi Qiu Y. Liu Zhizhen Qi W. Wang Zheng Kou

The subunit vaccine SV1 (20 μg F1+10 μg rV270) has been identified as the optimal formulation in mice, which provided a good protection against plague in mice, guinea pigs and rabbits. To compare SV1 and SV2 (200 μg F1+100 μg rV270) with live attenuated vaccine EV76, antibody responses, protective efficacy, cytokines (IFN-γ, TNF-α, IL-2, IL-4, IL-10 and IL-12) production, CD4/CD8 ratio and CD69(+) T-cell activation marker were determined in sera of the immunized Chinese-origin rhesus macaques, Macaca mulatta. The immunized animals with SV1 or SV2 developed higher anti-rV270 IgG titre, while those immunized with EV76 elicited a negligible IgG to V antigen, indicating that subunit vaccine (SV) had an advantage over EV76 in terms of the indispensable role of anti-V antibody against Yersinia pestis. There was no significant antibody titre difference between SV1 and SV2, suggesting that the immune response may have been saturated at the dose level of SV1. There were no statistical changes for CD4/CD8 ratios, IL-4 and CD69 levels between the three-vaccine immunized groups. However, a significant higher level of IL-12 was observed in the EV76 immunized animals, indicating that EV76 had an advantage over SV in respect of cellular immunity. Complete protection was observed for the immunized animals with SV and EV76, revealing that SV has a similar protective efficacy with EV76 against 6×10⁶ CFU of Y. pestis challenge by subcutaneous route in Chinese-origin rhesus macaques.

Yersinia pestis

Rhesus macaque

10.1111/j.1365-3083.2010.02456.x

Cite

Citations (33)

Genetic alterations in meningiomas of different textures

Gene (2016)

Dongxu Zhao Xiaochun Zhao Tao Liu Lei Chen Weizhen Gao

10.1016/j.gene.2016.07.057

Cite

Citations (3)