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| 1 | Blood-testis barrier and spermatogenesis: lessons From genetically-modified mice显示文摘血睾丸障碍(BTB ) 在它在生精的试管为 meiotic 和 postmeiotic 细菌房间的发展和成熟创造唯一的微型环境的睾丸在邻近的 Sertoli 房间之间被发现。它是复合 proteinous 结构,包括紧密的连接(TJ ) 的房间连接的几种类型镇静,粘附连接和差距连接(GJ ) 。一些 junctional 蛋白质作为 BTB 的结构的蛋白质工作,一些有规章的角色。删除或编码这些蛋白质的基因的功能的 silencing 可以破坏 BTB,它可以引起到 meiotic 和 postmeiotic 房间的免疫学的或另外的损坏并且最终导致 spermatogenic 拘捕和不孕。在这评论,我们将在 BTB 结构上总结调查结果并且从遗传上修改的老鼠模型工作并且讨论未来观点。 | Xiao-Hua Jiang Ihtisham Bukhari Wei Zheng Shi Yin Zheng Wang Howard J Cooke Qing-Hua Shi | 2014 | Asian Journal of Andrology2014，16，4： | 9 |
| 2 | TOL6BL突变导致减数分裂程序性DNA双链断裂无法产生和人类不孕显示文摘我们找到一个近亲婚配后代不育家系,该家系有3位非梗阻性无精子症患者和1位原因不明的女性不孕患者.全外显子组测序结合Sanger测序分析发现TOP6BL的c.483dup T突变在该家系中与不孕呈隐性共分离.正常的TOP6BL可与SPO11β结合进而导致减数分裂程序性DNA双链断裂(DSBs)产生,而该突变破坏了二者的结合.对家系中一位男患者的精母细胞进行分析,发现其同源染色体联会异常,减数分裂不能到达粗线期,且染色体轴上缺少减数分裂重组蛋白RPA和DMC1信号,表明其减数分裂程序性DSBs未能产生.我们制备了携带类似患者突变的小鼠,发现突变雄鼠具有与男患者相同的减数分裂异常,突变雌鼠不孕,其卵母细胞中程序性DSBs和减数分裂重组也不能发生,卵母细胞不能成熟.这些发现表明TOP6BL突变可导致人类不孕,为相关不孕不育患者的病因诊断和人工辅助生殖胚胎的遗传检查提供了分子标靶. | 焦玉莹 樊岁兴 Nazish Jabeen 张欢 Ranjha Khan Ghulam Murtaza 蒋涵玮 Asim Ali 李阳 鲍坚强 张贝贝 徐建泽 许波 Hafiz Muhammad Jafar Hussain Qumar Zaman Ihsan Khan Ihtisham Bukhari Furhan Iqbal Ayesha Yousaf Sobia Dil Manan Khan Niaz Ahmad 马慧 江小华 张远伟 史庆华 | 2020 | Science Bulletin2020，65，24： | 1 |
| 3 | NAD+associated genes as potential biomarkers for predicting the prognosis of gastric cancer显示文摘Nicotinamide adenine dinucleotide(NAD+)plays an essential role in cellular metabolism,mitochondrial homeostasis,inflammation,and senescence.However,the role of NAD+-regulated genes,including coding and long non-coding genes in cancer development is poorly understood.We constructed a prediction model based on the expression level of NAD+metabolism-related genes(NMRGs).Furthermore,we validated the expression of NMRGs in gastric cancer(GC)tissues and cell lines;additionally,β-nicotinamide mononucleotide(NMN),a precursor of NAD+,was used to treat the GC cell lines to analyze its effects on the expression level of NMRGs lncRNAs and cellular proliferation,cell cycle,apoptosis,and senescence-associated secretory phenotype(SASP).A total of 13 NMRGs-related lncRNAs were selected to construct prognostic risk signatures,and patients with high-risk scores had a poor prognosis.Some immune checkpoint genes were upregulated in the high-risk group.In addition,cell cycle,epigenetics,and senescence were significantly downregulated in the high-risk group.Notably,we found that the levels of immune cell infiltration,including CD8 T cells,CD4 naïve T cells,CD4 memory-activated T cells,B memory cells,and naïve B cells,were significantly associated with risk scores.Furthermore,the treatment of NMN showed increased proliferation of AGS and MKN45 cells.In addition,the expression of SASP factors(IL6,IL8,IL10,TGF-β,and TNF-α)was significantly decreased after NMN treatment.We conclude that the lncRNAs associated with NAD+metabolism can potentially be used as biomarkers for predicting clinical outcomes of GC patients. | XIANGDONG SUN HUIJUAN WEN FAZHAN LI IHTISHAM BUKHARI FEIFEI REN XIA XUE PENGYUAN ZHENG YANG MI | 2024 | Oncology Research2024，32，2： | 0 |
| 4 | cGAS regulates the DNA damage response to maintain proliferative signaling in gastric cancer cells显示文摘The activation of some oncogenes promote cancer cell proliferation and growth,facilitate cancer progression and metastasis by induce DNA replication stress,even genome instability.Activation of the cyclic GMP-AMP synthase(cGAS)mediates classical DNA sensing,is involved in genome instability,and is linked to various tumor development or therapy.However,the function of cGAS in gastric cancer remains elusive.In this study,the TCGA database and retrospective immunohistochemical analyses revealed substantially high cGAS expression in gastric cancer tissues and cell lines.By employing cGAS high-expression gastric cancer cell lines,including AGS and MKN45,ectopic silencing of cGAS caused a significant reduction in the proliferation of the cells,tumor growth,and mass in xenograft mice.Mechanistically,database analysis predicted a possible involvement of cGAS in the DNA damage response(DDR),further data through cells revealed protein interactions of the cGAS and MRE11-RAD50-NBN(MRN)complex,which activated cell cycle checkpoints,even increased genome instability in gastric cancer cells,thereby contributing to gastric cancer progression and sensitivity to treatment with DNA damaging agents.Furthermore,the upregulation of cGAS significantly exacerbated the prognosis of gastric cancer patients while improving radiotherapeutic outcomes.Therefore,we concluded that cGAS is involved in gastric cancer progression by fueling genome instability,implying that intervening in the cGAS pathway could be a practicable therapeutic approach for gastric cancer. | BIN LIU HAIPENG LIU FEIFEI REN HANGFAN LIU IHTISHAM BUKHARI YUMING FU WANQINGWU MINGHAI ZHAO SHAOGONG ZHU HUI MO FAZHAN LI MICHAEL B.ZHENG YOUCAI TANG PENGYUAN ZHENG YANG MI | 2021 | Oncology Research2021，29，2： | 0 |
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