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Protein & Cell

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ISSN 1674-800X (Print)
ISSN 1674-8018 (Online)
CN 11-5886/Q
Postal Subscription Code 80-984
2018 Impact Factor: 7.575

, Volume 10 Issue 9

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RECOLLECTION
COMMENTARY
RESEARCH ARTICLE
Mitochondrion-processed TERC regulates senescence without affecting telomerase activities
Qian Zheng, Peipei Liu, Ge Gao, Jiapei Yuan, Pengfeng Wang, Jinliang Huang, Leiming Xie, Xinping Lu, Fan Di, Tanjun Tong, Jun Chen, Zhi Lu, Jisong Guan, Geng Wang
Protein Cell. 2019, 10 (9): 631-648.  https://doi.org/10.1007/s13238-019-0612-5
Abstract   PDF (3470KB)

Mitochondrial dysfunctions play major roles in ageing. How mitochondrial stresses invoke downstream responses and how specificity of the signaling is achieved, however, remains unclear. We have previously discovered that the RNA component of Telomerase TERCis imported into mitochondria, processed to a shorter form TERC-53, and then exported back to the cytosol. Cytosolic TERC-53levels respond to mito- chondrial functions, but have no direct effect on these functions, suggesting that cytosolic TERC-53functions downstream of mitochondria as a signal of mitochon- drial functions. Here, we show that cytosolic TERC-53plays a regulatory role on cellular senescence and is involved in cognition decline in 10 months old mice, independent of its telomerase function. Manipulation of cytosolic TERC-53levels affects cellular senescence and cognition decline in 10 months old mouse hip-pocampi without affecting telomerase activity, and most importantly, affects cellular senescence in terc−/− cells. These findings uncover a senescence-related regulatory pathway with a non-coding RNA as the signal in mammals.

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Telomere-dependent and telomereindependent roles of RAP1 in regulating human stem cell homeostasis
Xing Zhang, Zunpeng Liu, Xiaoqian Liu, Si Wang, Yiyuan Zhang, Xiaojuan He, Shuhui Sun, Shuai Ma, Ng Shyh-Chang, Feng Liu, Qiang Wang, Xiaoqun Wang, Lin Liu, Weiqi Zhang, Moshi Song, Guang-Hui Liu, Jing Qu
Protein Cell. 2019, 10 (9): 649-667.  https://doi.org/10.1007/s13238-019-0610-7
Abstract   PDF (5564KB)

RAP1 is a well-known telomere-binding protein, but its functions in human stem cells have remained unclear. Here we generated RAP1-deficient human embryonic stem cells (hESCs) by using CRISPR/Cas9 technique and obtained RAP1-deficient human mesenchymal stem cells (hMSCs) and neural stem cells (hNSCs) via direc- ted differentiation. In both hMSCs and hNSCs, RAP1 not only negatively regulated telomere length but also acted as a transcriptional regulator of RELN by tuning the methylation status of its gene promoter. RAP1 defi- ciency enhanced self-renewal and delayed senescence in hMSCs, but not in hNSCs, suggesting complicated lineage-specific effects of RAP1 in adult stem cells. Altogether, these results demonstrate for the first time that RAP1 plays both telomeric and nontelomeric roles in regulating human stem cell homeostasis.

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Core pluripotency factors promote glycolysis of human embryonic stem cells by activating GLUT1 enhancer
Lili Yu, Kai-yuan Ji, Jian Zhang, Yanxia Xu, Yue Ying, Taoyi Mai, Shuxiang Xu, Qian-bing Zhang, Kai-tai Yao, Yang Xu
Protein Cell. 2019, 10 (9): 668-680.  https://doi.org/10.1007/s13238-019-0637-9
Abstract   PDF (2371KB)

Human embryonic stem cells (hESCs) depend on glycolysis for energy and substrates for biosynthesis. To understand the mechanisms governing the metabolism of hESCs, we investigated the transcriptional regulation of glucose transporter 1 (GLUT1, SLC2A1), a key glycolytic gene to maintain pluripotency. By combining the genome-wide data of binding sites of the core pluripotency factors (SOX2, OCT4, NANOG, denoted SON), chromosomal interaction and histone modification in hESCs, we identified a potential enhancer of the GLUT1 gene in hESCs, denoted GLUT1 enhancer (GE) element. GE interacts with the promoter of GLUT1, and the deletion of GE significantly reduces the expression of GLUT1, glucose uptake and glycolysis of hESCs, confirming that GE is an enhancer of GLUT1 in hESCs. In addition, the mutation of SON binding motifs within GE reduced the expression of GLUT1 as well as the interaction between GE and GLUT1 promoter, indicating that the binding of SON to GE is important for its activity. Therefore, SON promotes glucose uptake and glycolysis in hESCs by inducing GLUT1 expression through directly activating the enhancer of GLUT1.

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LETTER
Propofol reduces synaptic strength by inhibiting sodium and calcium channels at nerve terminals
Qing-Zhuo Liu, Mei Hao, Zi-Yang Zhou, Jian-Long Ge, Yi-Chen Wu, Ling-Ling Zhao, Xiang Wu, Yi Feng, Hong Gao, Shun Li, Lei Xue
Protein Cell. 2019, 10 (9): 688-693.  https://doi.org/10.1007/s13238-019-0624-1
Abstract   PDF (869KB)
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DNA-dependent protein kinase catalytic subunit (DNA-PKcs) contributes to incorporation of histone variant H2A.Z into nucleosomes
Ling-Yao Wang, Yun-xiao He, Min Li, Jian Ding, Yi Sui, Joan W. Conaway, Ronald C. Conaway, Fei Wang, Jingji Jin, Yong Cai
Protein Cell. 2019, 10 (9): 694-699.  https://doi.org/10.1007/s13238-019-0632-1
Abstract   PDF (913KB)
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CORRECTION
Correction to: Increasing targeting scope of adenosine base editors in mouse and rat embryos through fusion of TadA deaminase with Cas9 variants
Lei Yang, Xiaohui Zhang, Liren Wang, Shuming Yin, Biyun Zhu, Ling Xie, Qiuhui Duan, Huiqiong Hu, Rui Zheng, Yu Wei, Liangyue Peng, Honghui Han, Jiqin Zhang, Wenjuan Qiu, Hongquan Geng, Stefan Siwko, Xueli Zhang, Mingyao Liu, Dali Li
Protein Cell. 2019, 10 (9): 700-.  https://doi.org/10.1007/s13238-019-0631-2
Abstract   PDF (274KB)
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