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| 1 | Role ofthe IncRNA-p53 regulatory network in cancer显示文摘 | Ali Zhang Min Xu Yin-Yuan Mo | 2014 | Journal of Molecular Cell Biology2014，8，3： | 29 |
| 2 | The p53/miR-34 axis in development and disease显示文摘肿瘤 suppressor p53 是在人的癌症的最经常变异的基因之一。MicroRNAs (miRNAs ) 是在 post-transcriptional 水平上调整基因表示的小 non-proteincoding RNA。最近, p53 调整几 miRNAs 的 theexpression,这被显示出,从而代表 p53 发信号的重要机制。几个独立人士作为最流行的导致 p53 的 miRNAs 学习 miR-34 家庭的 identifiedthe 成员。miR-34s 经常是在 tumorentities 的变化的 silenced,建议他们是重要肿瘤 suppressors。确实, miR-34s 的宫外的表示禁止增长,对各种各样的癌症房间实体的间充质的转变,移植,侵略,和转移上皮。而且, miR-34 的 deliveryor 重新表示在癌症老鼠模型导致肿瘤生长和转移的著名压抑,并且可以 thereforerepresent 为未来癌症治疗学的有效策略。除他们在癌症的关键函数以外, themiR-34 家庭的成员也在精子发生,干细胞区别, neuronal 开发,老化,和 cardiovascularfunctions 起重要作用。因而, miR-34 也在各种各样的非癌的疾病被含有,例如大脑混乱,骨质疏松症,和心血管的复杂并发症。 | Matjaz Rokavec Huihui Li Longchang Jiang and Heiko Hermeking | 2014 | Journal of Molecular Cell Biology2014，8，3： | 27 |
| 3 | p53 modifications:exquisite decorations ofthe powerful guardian显示文摘The last 40 years have witnessed how p53 rose from a viral binding protein to a central factor in both stress responses and tumor suppression.The exquisite regulation of p53 functions is of vital importance for cell fate decisions.Among the multiple layers of mechanisms controlling p53 function,posttranslational modifications (PTMs) represent an efficient and precise way.Major p53 PTMs include phosphorylation,ubiquitination,acetylation,and methylation.Meanwhile,other PTMs like sumoylation,neddylation,O-GlcNAcylation,adenosine diphosphate (ADP)-ribosylation,hydroxylation,and p-hydroxybutyrylation are also shown to play various roles in p53 regulation.By independent action or interaction,PTMs affect p53 stability,conformation,localization,and binding partners.Deregulation of the PTM-related pathway is among the major causes of p53-associated developmental disorders or diseases,especially in cancers.This review focuses on the roles of different p53 modification types and shows how these modifications are orchestrated to produce various outcomes by modulating p53 activities or targeted to treat different diseases caused by p53 dysregulation. | Yanqing Liu Omid Tavana Wei Gu | 2019 | Journal of Molecular Cell Biology2019，11，7： | 24 |
| 4 | Mutant p53 in colon cancer显示文摘The accumulation of genetic alterations in driver genes is responsible for the development and malignant progression of colorectal cancer. Comprehensive genome analyses have revealed the driver genes, including APC, KRAS, TGFBR2, and TP53, whose mutations are frequently found in human colorectal cancers. Among them, the p53 mutation is found in ~60% of colorectal cancers, and a majority of mutations are missense-type at ‘hot spots’, suggesting an oncogenic role of mutant p53 by ‘gain-of-function’ mechanisms. Mouse model studies have shown that one of these missense-type mutations, p53 R270H (corresponding to human R273H), causes submucosal invasion of intestinal tumors, while the loss of wild-type p53 has a limited effect on the invasion process. Furthermore, the same mutant p53 promotes metastasis when combined with Kras activation and TGF-β suppression. Importantly, either missense-type p53 mutation or loss of wild-type p53 induces NF-κB activation by a variety of mechanisms, such as increasing promoter accessibility by chromatin remodeling, which may contribute to progression to epithelial–mesenchymal transition. These results indicate that missense-type p53 mutations together with loss of wild-type p53 accelerate the late stage of colorectal cancer progression through the activation of both oncogenic and inflammatory pathways. Accordingly, the suppression of the mutant p53 function via the inhibition of nuclear accumulation is expected to be an effective strategy against malignant progression of colorectal cancer. | Mizuho Nakayama Masanobu Oshima | 2019 | Journal of Molecular Cell Biology2019，11，4： | 22 |
| 5 | GSDMB promotes non-canonical pyroptosis by enhancing caspase-4 activity显示文摘Gasdermin B (GSDMB) has been reported to be associated with immune diseases in humans, but the detailed molecular mechanisms remain unsolved. The N-terminus of GSDMB by itself, unlike other gasdermin family proteins, does not induce cell death. Here, we show that GSDMB is highly expressed in the leukocytes of septic shock patients, which is associated with increased release of the gasdermin D (GSDMD) N-terminus. GSDMB expression and the accumulation of the N-terminal fragment of GSDMD are induced by the activation of the non-canonical pyroptosis pathway in a human monocyte cell line. The downregulation of GSDMB alleviates the cleavage of GSDMD and cell death. Consistently, the overexpression of GSDMB promotes GSDMD cleavage, accompanied by increased LDH release. We further found that GSDMB promotes caspase-4 activity, which is required for the cleavage of GSDMD in non-canonical pyroptosis, by directly binding to the CARD domain of caspase-4. Our study reveals a GSDMB-mediated novel regulatory mechanism for non-canonical pyroptosis and suggests a potential new strategy for the treatment of inflammatory diseases. | Qin Chen Peiliang Shi Yufang Wang Dayuan Zou Xiuwen Wu Dingyu Wang Qiongyuan Hu Yujie Zou Zan Huang Jianan Ren Zhaoyu Lin Xiang Gao | 2019 | Journal of Molecular Cell Biology2019，11，6： | 22 |
| 6 | Mitochondrial ROS promote macrophage pyroptosis by inducing GSDMD oxidation显示文摘Disrupted mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) generation are often associated with macrophage pyroptosis. It remains unclear how these forms of mitochondrial dysfunction relate to inflammasome activation and gasdermin-D (Gsdmd) cleavage, two central steps of the pyroptotic process. Here, we also found MMP collapse and ROS generation induced by Nlrp3 inflammasome activation as previous studies reported. The elimination of ROS alleviated the cleavage of Gsdmd, suggesting that Gsdmd cleavage occurs downstream of ROS release. Consistent with this result, hydrogen peroxide treatment augmented the cleavage of Gsdmd by caspase-1. Indeed, four amino acid residues of Gsdmd were oxidized under oxidative stress in macrophages. The efficiency of Gsdmd cleavage by inflammatory caspase-1 was dramatically reduced when oxidative modification was blocked by mutation of these amino acid residues. These results demonstrate that Gsdmd oxidation serves as a de novo mechanism by which mitochondrial ROS promote Nlrp3 inflammasome-dependent pyroptotic cell death. | Yufang Wang Peiliang Shi Qin Chen Zan Huang Dayuan Zou Jingzi Zhang Xiang Gao Zhaoyu Lin | 2019 | Journal of Molecular Cell Biology2019，11，12： | 23 |
| 7 | TRIM4 modulates type I interferon induction and cellular antiviral response by targeting RIG-I for K63-1inked ubiquitination显示文摘RIG-I 是认出病毒的 RNA 的不同种类的一个枢轴的细胞质的传感器。这识别导致抄写因素 NF-B 和 IRF3,它协作导致打的 activationof 我干扰素(IFN ) 和天生的抗病毒的 response.In 这研究,我们作为 RIG-I-mediated IFN 的一个积极管理者识别了整齐的家庭蛋白质 TRIM4 感应。Overexpressionof TRIM4 加强了 IRF3 和 NF-B 的被触发病毒的激活,以及 IFN- 正式就职,而 TRIM4had 相反的效果击倒。机械学地, TRIM4 与 RIG-I 联系并且为连接 K63 的 polyubiquitination 指向它。我们 TRIM4 是由调停的导致病毒的 IFN 正式就职小径的一个重要管理者的 findingsdemonstrate 为 K63-linkedubiquitination 的 RIG-I。 | Jie Yan Qi Li Ai-Ping Mao Hong-Bing Shu | 2014 | Journal of Molecular Cell Biology2014，8，2： | 21 |
| 8 | Cold adaptation in pigs depends on UCP3 in beige adipocytes显示文摘 | Jun Lin Chunwei Cao Cong Tao Rongcai Ye Meng Dong Qiantao Zheng Chao Wang Xiaoxiao Jiang Guosong Qin Changguo Yan Kui Li John R. Speakman Yanfang Wang Wanzhu Jin Jianguo Zhao | 2017 | Journal of Molecular Cell Biology2017，9，5： | 20 |
| 9 | p53 upregulated by HIF-la promotes hypoxiainduced G2/M arrest and renal fibrosis in vitro and in vivo显示文摘Hypoxia plays an important role in the genesis and progression of renal fibrosis.The underlying mechanisms, however, have not been sufficiently elucidated. We examined the role of p53 in hypoxia-induced renal fibrosis in cell culture (human and rat renal tubular epithelial cells) and a mouse unilateral ureteral obstruction (UUO) model. Cell cycle of tubular cells was determined by flow cytometry, and the expression of profibrogenic factors was determined by RT-PCR, immunohistochemistry, and western blotting. Chromatin immunoprecipitation and luciferase reporter experiments were performed to explore the effect of HIF-lα on p53 expression. We showed that, in hypoxic tubular cells, p53 upregulation suppressed the expression of CDK1 and cyclins Bl and DI, leading to cell cycle (G2/M) arrest (or delay) and higher expression of TGF-β, CTGF, collagens, and fibronectin. p53 suppression by siRNA or by a specific p53 inhibitor (PIF-α) triggered opposite effects preventing the G2/M arrest and profibrotic changes. In vivo experiments in the UUO model revealed similar antifibrotic results following intraperitoneal administration of PIF-α(2.2 mg/kg). Using gain-of-function, loss-of-function, and luciferase assays, we further identified an HRE3 region on the p53 promoter as the HIF-lα-binding site. The HIF-la-HRE3 binding resulted in a sharp transcriptional activation of p53. Collectively, we show the presence of a hypoxia-activated, p53-responsive profibrogenic pathway in the kidney. During hypoxia, p53 upregulation induced by HIF-la suppresses cell cycle progression, leading to the accumulation of G2/M cells, and activates profibrotic TGF-β and CTGF-mediated signaling pathways, causing extracellular matrix production and renal fibrosis. | Limin Liu Peng Zhang Ming Bai Lijie He Lei Zhang Ting Liu Zhen Yang Menglu Duan Minna Liu Baojian Liu Rui Du Qi Qian Shiren Sun | 2019 | Journal of Molecular Cell Biology2019，11，5： | 18 |
| 10 | Effective gene targeting in rabbits using RNA-guided Cas9 nucleases显示文摘 | Dongshan Yang Jie Xu Tianqing Zhu Jianglin Fan Liangxue Lai Jifeng Zhang Y. Eugene Chen | 2014 | Journal of Molecular Cell Biology2014，8，1： | 18 |
| 11 | Gain-of-function mutant p53 in cancer progression and therapy显示文摘p53 is a key tumor suppressor,and loss of p53 function is frequently a prerequisite for cancer development.The p53 gene is the most frequently mutated gene in human cancers;p53 mutations occur in>50%of all human cancers and in almost every type of human cancers.Most of p53 mutations in cancers are missense mutations,which produce the full-length mutant p53(mutp53)protein with only one amino acid difference from wild-type p53 protein.In addition to loss of the tumor-suppressive function of wild-type p53,many mutp53 proteins acquire new oncogenic activities independently of wild-type p53 to promote cancer progression,termed gain-of-function(GOF).Mutp53 protein often accumulates to very high levels in cancer cells,which is critical for its GOF.Given the high mutation frequency of the p53 gene and the GOF activities of mutp53 in cancer,therapies targeting mutp53 have attracted great interest.Further understanding the mechanisms underlying mutp53 protein accumulation and GOF will help develop effective therapies treating human cancers containing mutp53.In this review,we summarize the recent advances in the studies on mutp53 regulation and GOF as well as therapies targeting mutp53 in human cancers. | Cen Zhang Juan Liu Dandan Xu Tianliang Zhang Wenwei Hu Zhaohui Feng | 2020 | Journal of Molecular Cell Biology2020，12，9： | 18 |
| 12 | An HBV-encoded miRNA activates innate immunity to restrict HBV replication显示文摘We previously identified that hepatitis B virus(HBV)encodes a microRNA(HBV-miR-3)that restrains HBV replication by targeting the HBV transcript.However,whether HBV-miR-3 affects host innate immunity to modulate HBV replication remains unclear.Here,we examined the vital functions of HBV-miR-3 in the innate immune response after HBV infection.We found that HBV-miR-3 expression gradually increased in a dose-and time-dependent manner in HBV-infected HepG2-NTCP cells.HBV-miR-3 activated the JAK/STAT signaling pathway by downregulating SOCS5 in hepatocytes,thereby enhancing the IFN-induced anti-HBV effect.In addition,HBVmiR-3 in exosomes facilitated the Ml polarization of macrophages.Furthermore,exosomes containing HBV-miR-3 enhanced the secretion of IL-6 via inhibiting the SOCS5-mediated ubiquitination of EGFR.In short,these results demonstrate that HBV-miR-3 activates the innate immune response to restrain HBV replication by multiple pathways,which may suppress HBV-induced acute liver cell injury and affect the progression of persistent HBV infection. | Xiaoqing Zhao Lu Sun Ting Mu Jianying Yi Chaoqun Ma Hong Xie Min Liu Hua Tang | 2020 | Journal of Molecular Cell Biology2020，12，4： | 17 |
| 13 | miR-221/222 activate the Wnt/β-catenin signaling to promote triple-negative breast cancer显示文摘 | Sanhong Liu Zifeng Wang Zukai Liu Shuo Shi Zhaoran Zhang Jiawei Zhang Haifan Lin | 2018 | Journal of Molecular Cell Biology2018，10，4： | 16 |
| 14 | IRES-mediated cap-independent translation,a path leading to hidden proteome显示文摘Most eukaryotic mRNAs are translated in a cap-dependent fashion;however,under stress conditions,the cap-independent translation driven by internal ribosomal entry sites(IRESs)can serve as an alternative mechanism for protein production.Many IRESs have been discovered from viral or cellular mRNAs to promote ribosome assembly and initiate translation by recruiting different trons-acting factors.Although the mechanisms of translation initiation driven by viral IRESs are relatively well understood,the existence of cellular IRESs is still under debate due to the limitations of translation reporter systems used to assay IRES activities.A recent screen identified>1000 putative IRESs from viral and human mRNAs,expanding the scope and mechanism for capindependent translation.Additionally,a large number of circular RNAs lacking free ends were identified in eukaryotic cells,many of which are found to be translated through IRESs.These findings suggest that IRESs may play a previously unappreciated role in driving translation of the new type of mRNA,implying a hidden proteome produced from cap-independent translation. | Yun Yang Zefeng Wang | 2019 | Journal of Molecular Cell Biology2019，11，10： | 16 |
| 15 | Understanding p53 functions through p53 antibodies显示文摘TP53 is the most frequently mutated gene across all cancer types. Our understanding of its functions has evolved since its discovery four decades ago. Initially thought to be an oncogene, it was later realized to be a critical tumour suppressor. A significant amount of our knowledge about p53 functions have come from the use of antibodies against its various forms. The early anti-p53 antibodies contributed to the recognition of p53 accumulation as a common feature of cancer cells and to our understanding of p53 DNA-binding and transcription activities. They led to the concept that conformational changes can facilitate p53’s activity as a growth inhibitory protein. The ensuing p53 conformational-specific antibodies further underlined p53’s conformational flexibility, collectively forming the basis for current efforts to generate therapeutic molecules capable of altering the conformation of mutant p53. A subsequent barrage of antibodies against post-translational modifications on p53 has clarified p53’s roles further, especially with respect to the mechanistic details and context-dependence of its activity. More recently, the generation of p53 mutation-specific antibodies have highlighted the possibility to go beyond the general framework of our comprehension of mutant p53-and promises to provide insights into the specific properties of individual p53 mutants. This review summarizes our current knowledge of p53 functions derived through the major classes of anti-p53 antibodies, which could be a paradigm for understanding other molecular events in health and disease. | Kanaga Sabapathy David P.Lane | 2019 | Journal of Molecular Cell Biology2019，11，4： | 15 |
| 16 | COL4A3 mutations cause focal segmenta glomerulosclerosis显示文摘 | Jingyuan Xie Xiaoxi Wu Hong Ren Weiming Wang Zhaohui Wang Xiaoxia Pan Xu Hao Jun Tong Jun Ma Zhibin Ye Guoyu Meng Yufei Zhu Krzysztof Kiryluk Xiangyin Kong Landian Hu Nan Chen | 2014 | Journal of Molecular Cell Biology2014，8，6： | 15 |
| 17 | AMPK activation by peri-sciatic nerve administration of ozone attenuates CCl-induced neuropathic pain in rats显示文摘 | Lijuan Lu Cailong Pan Lu Chen Liang Hu Chaoyu Wang Yuan Han Yanjing Yang Zhixiang Cheng Wen-Tao Liu | 2017 | Journal of Molecular Cell Biology2017，9，2： | 14 |
| 18 | Adiponectin signaling and function in insulin target tissues显示文摘Obesity-linked type 2 diabetes is one of the paramount causes of morbidity and mortality worldwide,posing a major threat on human health,productivity,and quality of life.Despite great progressmadetowards a better understanding of the molecular basis of diabetes,the available clinical counter-measures against insulin resistance,a defect that is central to obesity-linked type 2 diabetes,remain inadequate.Adiponectin,an abundant adipocyte-secreted factor with a wide-range of biological activities,improves insulin sensitivity in major insulin target tissues,modulates inflammatory responses,and plays a crucial role in the regulation of energy metabolism.However,adiponectin as a promising therapeutic approach has not been thoroughly explored in the context of pharmacological intervention,and extensive efforts are being devoted to gain mechanistic understanding of adiponectin signaling and its regulation,and reveal therapeutic targets.Here,we discuss tissue-and cell-specific functions of adiponectin,with an emphasis on the regulation of adiponectin signaling pathways,and the potential crosstalk between the adiponectin and other signaling pathways involved in metabolic regulation.Understanding better just why and how adiponectin and its downstream effector molecules work will be essential,together with empirical trials,to guide us to therapies that target the root cause(s)of type 2 diabetes and insulin resistance. | Hong Ruan Lily Q.Dong | 2016 | Journal of Molecular Cell Biology2016，8，2： | 14 |
| 19 | Wnt signaling in the nervous system and in Alzheimer's disease显示文摘Wnts 包括出现了是包括 organogenesis,中脑发展以及干细胞增长调整几 aspectsof 开发的发信号的串联的部分的蛋白质的一个大家庭。在在成年大脑的 neuronal 电路并且也的发展的 Wnt 发信号小径 playsdifferent 角色,在它调整 synaptic transmissionand 的地方粘性。它也包括癌症和 neurodegenerative 疾病在各种各样的疾病被含有,在基本生物过程的 reflectingits 关联。这评论与 Alzheimer 的疾病(广告) 的一个焦点在成熟 nervoussystem 关于 Wnts 功能总结进步。我们讨论正规的 modulating 和不在经典中的 Wnt signalingas 的前景为 neuroprotection 的策略。这将包括 Wnts 的潜力到:是的(i) 行为在学习和记忆的 hippocampalsynapses 和影响的有势力管理者;(ii ) 调整成年神经发生;并且(iii ) 最后控制广告致病。 | Nibaldo C. Inestrosa Lorena Varela-Nallar | 2014 | Journal of Molecular Cell Biology2014，8，1： | 14 |
| 20 | The hidden switches undertying RORα-mediated circuits that critically regulate uncontrolled cell proliferation显示文摘 | Dongkwan Shin Ik Soo Kim Ji Min Lee Sung-Young Shin Jong-Hoon Lee Sung Hee Baek Kwang-Hyun Cho | 2014 | Journal of Molecular Cell Biology2014，8，4： | 13 |
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