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Regulation of Alternative Splicing of Human Tau Exon 10 by Phosphorylation of Splicing Factors

机译：剪接因子磷酸化对人Tau外显子10选择性剪接的调控

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Hartmann Annette M.; Rujescu Dan; Giannakouros Thomas; Nikolakaki Eleni; Goedert Michel; Mandelkow Eva-Maria; Gao Qing Sheng; Andreadis Athena; Stamm Stefan;
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年度 2001
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正文语种 eng
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1. Regulation of alternative splicing of human tau exon 10 by phosphorylation of splicing factors. [J] . Hartmann AM, Rujescu D, Giannakouros T, Molecular and cellular neurosciences . 2001,第1期

机译：通过剪接因子的磷酸化调节人tau外显子10的剪接。
2. COMPREHENSIVE UNDERSTANDING OF TAU EXON 10 ALTERNATIVE SPLICING REGULATION [J] . Sansi Xing, Yu Lu Alzheimer’s & dementia: the journal of the Alzheimer’s Association . 2018,第7期

机译：综合了解TAU EXON 10替代剪接规范
3. Regulation of alternative splicing of tau exon 10 by 9G8 and Dyrk1A [J] . DingS., ShiJ., QianW., Neurobiology of Aging: Experimental and Clinical Research . 2012,第7期

机译：9G8和Dyrk1A对tau外显子10选择性剪接的调控
4. A New Transcript Splice Variant of the Human Glucocorticoid Receptor: Identification and Tissue Distribution of hGR△313-338, an Alternative Exon 2 Transactivation Domain Isoform [C] . JONATHAN D. TURNER, ANDREA B. SCHOTE, MARC KEIPES, Meeting on Cell Signaling World: Signal Transduction Pathways as Therapeutic Targets . 2007

机译：人糖皮质激素受体的一个新的转录剪接变体：hGR△313-338，另一外显子2反式激活域同工型的鉴定和组织分布。
5. Exosomal proteome changes induced by human tau expression are modulated by the presence of the microtubule-binding domain and alternatively spliced exons 2-3 in SH-SY5Y neuroblastoma cells [D] . Aladwan, Mohammad Mahmoud. 2017

机译：SH-SY5Y神经母细胞瘤细胞中微管结合结构域的存在和其他剪接的外显子2-3的存在可以调节人tau表达诱导的外泌体蛋白质组变化
6. hnRNP A1 Regulates Alternative Splicing of Tau Exon 10 by Targeting 3′ Splice Sites [O] . Yongchao Liu, Donggun Kim, Namjeong Choi, 2020

机译：hnRNP A1通过靶向3剪接位点调控Tau外显子10的选择性剪接
7. Regulation of Alternative Splicing of Human Tau Exon 10 by Phosphorylation of Splicing Factors [O] . Annette M. Hartmann, Dan Rujescu, Thomas Giannakouros, 2013

机译：通过剪接因子的磷酸化调节人Tau外显子10的可变剪接

Regulation of Alternative Splicing of Human Tau Exon 10 by Phosphorylation of Splicing Factors

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