Supplementary File 1-12

The Datasets Serve for the Misssion of Finding Convergent Transcriptomic Evidence about Dysfunctional Quantitative Mechanism of Synaptic Plasticity Control in ASD. Including: Supplementary File 1 Composition of nodes in Signal Network.xlsxSupplementary File 2 Regulation edges in Signal Network.xlsx Supplementary File 3 Syngo_annotations.xlsx Supplementary File 4 Annotation_SIGNOR and SignaLink_Omnipath.xlsx Supplementary File 5 mSiReN - network structure overall.csv Supplementary File 6 The activated nodes and edges from NIVaCaR.xlsx Supplementary File 7 Nodes Information and DE analysis about translation control and LTP or LTD related proteins and complexes.xlsx Supplementary File 8 ProComReN weights in best model.xlsx Supplementary File 9 The variation (sd) for cell types.xlsx Supplementary File 10 Targeted ncRNA with sub-pathway nodes.xlsx Supplementary File 11 String interactions with sub-pathway nodes.xlsx Supplementary File 12 SFARI with sub-pathway nodes.xlsx<br>

本数据集旨在服务于探寻自闭症谱系障碍（ASD, Autism Spectrum Disorder）中突触可塑性调控功能失调量化机制的收敛性转录组学证据这一研究任务。包含如下补充文件：
1. 补充文件1：信号网络节点构成.xlsx
2. 补充文件2：信号网络调控边.xlsx
3. 补充文件3：Syngo注释文件.xlsx
4. 补充文件4：SIGNOR与SignaLink_Omnipath注释文件.xlsx
5. 补充文件5：mSiReN整体网络结构.csv
6. 补充文件6：来自NIVaCaR的激活节点与边.xlsx
7. 补充文件7：翻译调控及长时程增强（LTP, Long-term Potentiation）、长时程抑制（LTD, Long-term Depression）相关蛋白与复合物的节点信息及差异表达分析.xlsx
8. 补充文件8：最优模型中的ProComReN权重.xlsx
9. 补充文件9：细胞类型的变异（标准差，sd）.xlsx
10. 补充文件10：携带亚通路节点的靶向非编码RNA（ncRNA, non-coding RNA）.xlsx
11. 补充文件11：与亚通路节点关联的STRING相互作用数据集.xlsx
12. 补充文件12：携带亚通路节点的SFARI数据集.xlsx