Recollection
Professor Tafu Yu: an eminent agricultural scientist and outstanding educator of our nation
Shuang Zhao, Tiantian Xu, Hexiang Wang
2019, 10(8): 545-549.   doi: 10.1007/s13238-017-0494-3
[Abstract](4) [PDF 1332KB](331)
Abstract:
Review
Sialylation is involved in cell fate decision during development, reprogramming and cancer progression
Fenjie Li, Junjun Ding
2019, 10(8): 550-565.   doi: 10.1007/s13238-018-0597-5
[Abstract](4) [PDF 1372KB](1)
Abstract:
Sialylation, or the covalent addition of sialic acid to the terminal end of glycoproteins, is a biologically important modification that is involved in embryonic development, neurodevelopment, reprogramming, oncogenesis and immune responses. In this review, we have given a comprehensive overview of the current literature on the involvement of sialylation in cell fate decision during development, reprogramming and cancer progression. Sialylation is essential for early embryonic development and the deletion of UDP-GlcNAc 2-epimerase, a rate-limiting enzyme in sialic acid biosynthesis, is embryonically lethal. Furthermore, the sialyltransferase ST6GAL1 is required for somatic cell reprogramming, and its downregulation is associated with decreased reprogramming efficiency. In addition, sialylation levels and patterns are altered during cancer progression, indicating the potential of sialylated molecules as cancer biomarkers. Taken together, the current evidences demonstrate that sialylation is involved in crucial cell fate decision.
Research Articles
Unbiased transcriptomic analyses reveal distinct effects of immune defciency in CNS function with and without injury
Dandan Luo, Weihong Ge, Xiao Hu, Chen Li, Chia-Ming Lee, Liqiang Zhou, Zhourui Wu, Juehua Yu, Sheng Lin, Jing Yu, Wei Xu, Lei Chen, Chong Zhang, Kun Jiang, Xingfei Zhu, Haotian Li, Xinpei Gao, Yanan Geng, Bo Jing, Zhen Wang, Changhong Zheng, Rongrong Zhu, Qiao Yan, Quan Lin, Keqiang Ye, Yi E. Sun, Liming Cheng
2019, 10(8): 566-582.   doi: 10.1007/s13238-018-0559-y
[Abstract](12) [PDF 5901KB](477)
Abstract:
The mammalian central nervous system (CNS) is considered an immune privileged system as it is separated from the periphery by the blood brain barrier (BBB). Yet, immune functions have been postulated to heavily influence the functional state of the CNS, especially after injury or during neurodegeneration. There is controversy regarding whether adaptive immune responses are beneficial or detrimental to CNS injury repair. In this study, we utilized immunocompromised SCID mice and subjected them to spinal cord injury (SCI). We analyzed motor function, electrophysiology, histochemistry, and performed unbiased RNA-sequencing. SCID mice displayed improved CNS functional recovery compared to WT mice after SCI. Weighted gene-coexpression network analysis (WGCNA) of spinal cord transcriptomes revealed that SCID mice had reduced expression of immune function-related genes and heightened expression of neural transmission-related genes after SCI, which was confirmed by immunohistochemical analysis and was consistent with better functional recovery. Transcriptomic analyses also indicated heightened expression of neurotransmission-related genes before injury in SCID mice, suggesting that a steady state of immune-deficiency potentially led to CNS hyper-connectivity. Consequently, SCID mice without injury demonstrated worse performance in Morris water maze test. Taken together, not only reduced inflammation after injury but also dampened steady-state immune function without injury heightened the neurotransmission program, resulting in better or worse behavioral outcomes respectively. This study revealed the intricate relationship between immune and nervous systems, raising the possibility for therapeutic manipulation of neural function via immune modulation.
PKM2 coordinates glycolysis with mitochondrial fusion and oxidative phosphorylation
Tong Li, Jinbo Han, Liangjie Jia, Xiao Hu, Liqun Chen, Yiguo Wang
2019, 10(8): 583-594.   doi: 10.1007/s13238-019-0618-z
[Abstract](18) [PDF 1310KB](2)
Abstract:
A change in the metabolic flux of glucose from mitochondrial oxidative phosphorylation (OXPHOS) to aerobic glycolysis is regarded as one hallmark of cancer. However, the mechanisms underlying the metabolic switch between aerobic glycolysis and OXPHOS are unclear. Here we show that the M2 isoform of pyruvate kinase (PKM2), one of the rate-limiting enzymes in glycolysis, interacts with mitofusin 2 (MFN2), a key regulator of mitochondrial fusion, to promote mitochondrial fusion and OXPHOS, and attenuate glycolysis. mTOR increases the PKM2:MFN2 interaction by phosphorylating MFN2 and thereby modulates the effect of PKM2:MFN2 on glycolysis, mitochondrial fusion and OXPHOS. Thus, an mTOR-MFN2-PKM2 signaling axis couples glycolysis and OXPHOS to modulate cancer cell growth.
A miRNA-HERC4 pathway promotes breast tumorigenesis by inactivating tumor suppressor LATS1
Youqin Xu, Kaiyuan Ji, Meng Wu, Bingtao Hao, Kai-tai Yao, Yang Xu
2019, 10(8): 595-605.   doi: 10.1007/s13238-019-0607-2
[Abstract](9) [PDF 2639KB](2)
Abstract:
The E3 ligase HERC4 is overexpressed in human breast cancer and its expression levels correlated with the prognosis of breast cancer patients. However, the roles of HERC4 in mammary tumorigenesis remain unclear. Here we demonstrate that the knockdown of HERC4 in human breast cancer cells dramatically suppressed their proliferation, survival, migration, and tumor growth in vivo, while the overexpression of HERC4 promoted their aggressive tumorigenic activities. HERC4 is a new E3 ligase for the tumor suppressor LATS1 and destabilizes LATS1 by promoting the ubiquitination of LATS1. miRNA-136-5p and miRNA-1285-5p, expression of which is decreased in human breast cancers and is inversely correlated with the prognosis of breast cancer patients, are directly involved in suppressing the expression of HERC4. In summary, we discover a miRNA-HERC4- LATS1 pathway that plays important roles in the pathogenesis of breast cancer and represents new therapeutic targets for human breast cancer.
Letters
Developing potent PROTACs tools for selective degradation of HDAC6 protein
Zixuan An, Wenxing Lv, Shang Su, Wei Wu, Yu Rao
2019, 10(8): 606-609.   doi: 10.1007/s13238-018-0602-z
[Abstract](25) [PDF 986KB](16)
Abstract:
VHL-1 inactivation and mitochondrial antioxidants rescue C. elegans dopaminergic neurodegeneration
Song Chen, Shuo Luo, Zhe Zhang, Dengke K. Ma
2019, 10(8): 610-614.   doi: 10.1007/s13238-019-0621-4
[Abstract](1) [PDF 2165KB](0)
Abstract:
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ATP6V0d2 mediates leucine-induced mTORC1 activation and polarization of macrophages
Pingfei Li, Xiaofei Deng, Jing Luo, Yufei Chen, Guoyu Bi, Feili Gong, Zhengping Wei, Na Liu, Huabin Li, Arian Laurence, Xiang-Ping Yang
2019, 10(8): 615-619.   doi: 10.1007/s13238-019-0636-x
[Abstract](0) [PDF 868KB](0)
Abstract:
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Correction to: Glycosylation of dentin matrix protein 1 is a novel key element for astrocyte maturation and BBB integrity
Bo Jing, Chunxue Zhang, Xianjun Liu, Liqiang Zhou, Jiping Liu, Yinan Yao, Juehua Yu, Yuteng Weng, Min Pan, Jie Liu, Zuolin Wang, Yao Sun, Yi Eve Sun
2019, 10(8): 620-621.   doi: 10.1007/s13238-018-0574-z
[Abstract](3) [PDF 864KB](192)
Abstract:
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Current issue
  • ISSN1674-800X
  • EISSN1674-8018
  • IF (2018) 7.575

Microbiota and Human Health

May 2018
Volume 9
Issue 5
pp: 395-510

Metabolism and Disease

May 2018
Volume 9
Issue 2
pp: 141-237

Therapeutic Antibodies

May 2018
Volume 9
Issue 1
pp: 1-139

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