Junbo Liang

Chinese Academy of Medical Sciences & Peking Union Medical College

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Shiying Miao

Chinese Academy of Medical Sciences & Peking Union Medical College

Longchang Xu

Chinese Academy of Medical Sciences & Peking Union Medical College

Linfang Wang

Shanxi Agricultural University

Mengmeng Zhang

Chinese Academy of Medical Sciences & Peking Union Medical College

Jie Wang

Tianjin Polytechnic University

Hailong Wang

Foshan University

Chunyang Xiong

Peking University

Liang Guo

Harbin Institute of Technology

Di-Hua Cao

Guangzhou First People's Hospital

Wenjie Liu

Guangdong Pharmaceutical University

Cooperative Institutions

Chinese Academy of Medical Sciences & Peking Union Medical College

Peking Union Medical College Hospital

Peking University

Shanxi Medical University

Tsinghua University

University of Chinese Academy of Sciences

Chinese Academy of Sciences

Guangzhou Medical University

South China University of Technology

Sun Yat-sen University

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Small Kinetochore Associated Protein (SKAP) Promotes UV-Induced Cell Apoptosis through Negatively Regulating Pre-mRNA Processing Factor 19 (Prp19)

PLoS ONE (2014)

Shan Lu Renxian Wang Congli Cai Junbo Liang Longchang Xu

Apoptosis is a regulated cellular suicide program that is critical for the development and maintenance of healthy tissues. Previous studies have shown that small kinetochore associated protein (SKAP) cooperates with kinetochore and mitotic spindle proteins to regulate mitosis. However, the role of SKAP in apoptosis has not been investigated. We have identified a new interaction involving SKAP, and we propose a mechanism through which SKAP regulates cell apoptosis. Our experiments demonstrate that both overexpression and knockdown of SKAP sensitize cells to UV-induced apoptosis. Further study has revealed that SKAP interacts with Pre-mRNA processing Factor 19 (Prp19). We find that UV-induced apoptosis can be inhibited by ectopic expression of Prp19, whereas silencing Prp19 has the opposite effect. Additionally, SKAP negatively regulates the protein levels of Prp19, whereas Prp19 does not alter SKAP expression. Finally, rescue experiments demonstrate that the pro-apoptotic role of SKAP is executed through Prp19. Taken together, these findings suggest that SKAP promotes UV-induced cell apoptosis by negatively regulating the anti-apoptotic protein Prp19.

Ectopic expression

10.1371/journal.pone.0092712

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Citations (8)

Seasonal artificial neural network model for water quality prediction via a clustering analysis method in a wastewater treatment plant of China

Desalination and Water Treatment (2014)

Ying Zhao Liang Guo Junbo Liang Min Zhang

For recovering the water quality of a river, it is a key factor to improve purifying capacity of wastewater in wastewater treatment plants (WTPs). The relational model for some key parameters of WTP processes is important for it can reveal the current situation and handling ability of the WTP and offer managers more useful information to design the processes for the optimized operation. The seasonal artificial neural network (ANN) models were designed for improving purifying ability of wastewater in a WTP of Harbin, northeast of China. The ANN models revealed the relationship of raw water quality, energy consumption, and effluent water quality. The effluent water quality could be predicted by the models. The clustering analysis method, an important data mining method, was used to classify the WTP data for building seasonal models. Meanwhile, an annual model was built by the whole data. It indicates that the prediction accuracy of seasonal models is better than the annual model by contrasting the errors. Seasonal models should be a more effective tool to reveal the relationship of WTP data. So it can offer managers more precise information to control and design the processes of WTPs, which result in better purifying ability of wastewater.

10.1080/19443994.2014.986202

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Citations (25)

Rhomboid domain containing 1 promotes colorectal cancer growth through activation of the EGFR signalling pathway

Nature Communications (2015)

Wei Song Wenjie Liu Hong Zhao Shangze Li Xin Guan

Abstract Rhomboid proteins perform a wide range of important functions in a variety of organisms. Recent studies have revealed that rhomboid proteins are involved in human cancer progression; however, the underlying molecular mechanism remains largely unclear. Here we show that RHBDD1, a rhomboid intramembrane serine protease, is highly expressed and closely associated with survival in patients with colorectal cancer. We observe that inactivation of RHBDD1 decreases tumor cell growth. Further studies show that RHBDD1 interacts with proTGFα and induces the ADAM-independent cleavage and secretion of proTGFα. The secreted TGFα further triggers the activation of the EGFR/Raf/MEK/ERK signalling pathway. Finally, the positive correlation of RHBDD1 expression with the EGFR/Raf/MEK/ERK signalling pathway is further corroborated in a murine model of colitis-associated colorectal cancer. These findings provide evidence of a growth-promoting role for RHBDD1 in colorectal cancer and may aid the development of tumor biomarkers or antitumor therapeutics.

Rhomboid

10.1038/ncomms9022

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Citations (73)

Suppression of non-muscle myosin II boosts T cell cytotoxicity against tumors

Science Advances (2024)

Yingyun Yang Dahan Wen Feng Lin Xiaowei Song Ruiyang Pang

Increasing evidence highlights the importance of immune mechanoregulation in establishing and sustaining tumor-specific cytotoxicity required for desirable immunotherapeutic outcomes. However, the molecular connections between mechanobiological inputs and outputs and the designated immune activities remain largely unclear. Here, we show that partial inhibition of non-muscle myosin II (NM II) augmented the traction force exerted by T cells and potentiated T cell cytotoxicity against tumors. By using T cells from mice and patients with cancer, we found that NM II is required for the activity of NKX3-2 in maintaining the expression of ADGRB3, which shapes the filamentous actin (F-actin) organization and ultimately attributes to the reduced traction force of T cells in the tumor microenvironment. In animal models, suppressing the NM II-NKX3-2-ADGRB3 pathway in T cells effectively suppressed tumor growth and improved the efficacy of the checkpoint-specific immunotherapy. Overall, this work provides insights into the biomechanical regulation of T cell cytotoxicity that can be exploited to optimize clinical immunotherapies.

10.1126/sciadv.adp0631

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A ruthenium(II) complex binds protein and inhibits proliferation and induces apoptosis in human gastric cancer SGC-7901 cells

Polyhedron (2015)

Sihong Liu Hui-Hua Xu Jianwei Zhu Yan Wang Yamin Liu

HeLa

Bovine serum albumin

MTT assay

10.1016/j.poly.2015.11.052

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Citations (3)

Toxicity of microcystins in the isolated hepatocytes of common carp (Cyprinus carpio L.)

Ecotoxicology and Environmental Safety (2006)

Xiaoyu Li Jie Wang Junbo Liang Yongding Liu

Microcystin-LR

Agarose gel electrophoresis

Common carp

Microcystis aeruginosa

10.1016/j.ecoenv.2006.10.003

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Citations (23)

Ubiquitylation of Rad51d Mediated by E3 Ligase Rnf138 Promotes the Homologous Recombination Repair Pathway

PLoS ONE (2016)

Deqiang Han Junbo Liang Yalan Lu Longchang Xu Shiying Miao

Ubiquitylation has an important role as a signal transducer that regulates protein function, subcellular localization, or stability during the DNA damage response. In this study, we show that Ring domain E3 ubiquitin ligases RNF138 is recruited to DNA damage site quickly. And the recruitment is mediated through its Zinc finger domains. We further confirm that RNF138 is phosphorylated by ATM at Ser124. However, the phosphorylation was dispensable for recruitment to the DNA damage site. Our findings also indicate that RAD51 assembly at DSB sites following irradiation is dramatically affected in RNF138-deficient cells. Hence, RNF138 is likely involved in regulating homologous recombination repair pathway. Consistently, efficiency of homologous recombination decreased observably in RNF138-depleted cells. In addition, RNF138-deficient cell is hypersensitive to DNA damage insults, such as IR and MMS. And the comet assay confirmed that RNF138 directly participated in DNA damage repair. Moreover, we find that RAD51D directly interacted with RNF138. And the recruitment of RAD51D to DNA damage site is delayed and unstable in RNF138-depleted cells. Taken together, these results suggest that RNF138 promotes the homologous recombination repair pathway.

Non-homologous end joining

Comet Assay

Homology directed repair

10.1371/journal.pone.0155476

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Citations (11)

The Ankyrin Repeat Domain 49 (ANKRD49) Augments Autophagy of Serum-Starved GC-1 Cells through the NF-κB Pathway

PLoS ONE (2015)

Hailong Wang Shasha Fan Min Pang Yiheng Liu Min Guo

The ankyrin repeat domain 49 (ANKRD49) is an evolutionarily conserved protein highly expressed in testes. However, the function of ANKRD49 in spermatogenesis is unknown. In this study, we found that ANKRD49 resides primarily in nucleus of spermatogonia, spermatocytes and round spermatids. ANKRD49 overexpression augments starvation-induced autophagy in male germ GC-1 cells whereas shRNA knockdown of ANKRD49 attenuates the autophagy. Inhibition of NF-κB pathway by its inhibitors or p65 siRNA prevents the ANKRD49-dependent autophagy augmentation, demonstrating that ANKRD49 enhances autophagy via NF-κB pathway. Our findings suggest that ANKRD49 plays an important role in spermatogenesis via promotion of autophagy-dependent survival.

Ankyrin repeat

Ankyrin

BAG3

10.1371/journal.pone.0128551

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Citations (15)