Supporting Information (PDF). We inadvertently included the incorrect ¹H NMR and ¹³C NMR spectra for compounds YT117R and YT117S. We have updated the Supporting Information with the correct spectra and also included chiral supercritical fluid chromatography traces for these compounds. We also corrected the compound numbers in Figure S6 to read YT47R and YT47S. The Supporting Information is available free of charge at https://pubs.acs.org/doi/10.1021/jacs.3c05058. Computational model showing the stereoselective engagement of DCAF1_C1113 by MY-1B; computational model of conjugation strategies of the MY-1B core scaffold; abolishing DCAF1 engagement by switching acrylamide to butynamide; concentration-dependent and time-dependent degradation of FKBP12 by DCAF1-directed electrophilic PROTACs; degradation of recombinantly expressed HA-FKBP12, of endogenous FKBP12, and of endogenous BRD4 by DCAF1-directed electrophilic PROTACs; comparing DCAF1 engagement by YT117R and YT47R; binding of DCAF1 near C1113 by a reversible small molecule CYCA-117-70; list of proteins showing substantial and significant changes in abundance in YT47-treated HEK293T cells; biological materials and methods; whole gels and Western blots; and synthetic chemistry (corrected) (PDF) Most electronic Supporting Information files are available without a subscription to ACS Web Editions. Such files may be downloaded by article for research use (if there is a public use license linked to the relevant article, that license may permit other uses). Permission may be obtained from ACS for other uses through requests via the RightsLink permission system: http://pubs.acs.org/page/copyright/permissions.html. This article has not yet been cited by other publications. The Supporting Information is available free of charge at https://pubs.acs.org/doi/10.1021/jacs.3c05058. Computational model showing the stereoselective engagement of DCAF1_C1113 by MY-1B; computational model of conjugation strategies of the MY-1B core scaffold; abolishing DCAF1 engagement by switching acrylamide to butynamide; concentration-dependent and time-dependent degradation of FKBP12 by DCAF1-directed electrophilic PROTACs; degradation of recombinantly expressed HA-FKBP12, of endogenous FKBP12, and of endogenous BRD4 by DCAF1-directed electrophilic PROTACs; comparing DCAF1 engagement by YT117R and YT47R; binding of DCAF1 near C1113 by a reversible small molecule CYCA-117-70; list of proteins showing substantial and significant changes in abundance in YT47-treated HEK293T cells; biological materials and methods; whole gels and Western blots; and synthetic chemistry (corrected) (PDF) Most electronic Supporting Information files are available without a subscription to ACS Web Editions. Such files may be downloaded by article for research use (if there is a public use license linked to the relevant article, that license may permit other uses). Permission may be obtained from ACS for other uses through requests via the RightsLink permission system: http://pubs.acs.org/page/copyright/permissions.html.

中文翻译：

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更正“通过立体选择性和位点特异性参与 DCAF1 的亲电 PROTAC 降解靶向蛋白质”

支持信息 (PDF)。我们无意中包含了不正确的¹ H NMR 和¹³化合物 YT117R 和 YT117S 的 C NMR 光谱。我们用正确的光谱更新了支持信息，还包括这些化合物的手性超临界流体色谱图。我们还更正了图 S6 中的化合物编号以读取 YT47R 和 YT47S。支持信息可在 https://pubs.acs.org/doi/10.1021/jacs.3c05058 免费获得。显示 MY-1B 对 DCAF1_C1113 的立体选择性参与的计算模型；MY-1B核心支架结合策略的计算模型；通过将丙烯酰胺转换为丁炔酰胺来取消 DCAF1 的参与；DCAF1 定向亲电 PROTAC 对 FKBP12 的浓度依赖性和时间依赖性降解；DCAF1 定向亲电 PROTAC 降解重组表达的 HA-FKBP12、内源性 FKBP12 和内源性 BRD4；比较 YT117R 和 YT47R 对 DCAF1 的参与；通过可逆小分子 CYCA-117-70 在 C1113 附近结合 DCAF1；在经 YT47 处理的 HEK293T 细胞中显示大量显着变化的蛋白质列表；生物材料和方法；全凝胶和蛋白质印迹；和合成化学（已更正）(PDF) 大多数电子支持信息文件无需订阅 ACS 网络版即可获得。此类文件可以按文章下载以供研究使用（如果相关文章有链接的公共使用许可，则该许可可能允许其他用途）。可以通过 RightsLink 许可系统请求从 ACS 获得用于其他用途的许可：http://pubs.acs.org/page/copyright/permissions.html。这篇文章尚未被其他出版物引用。支持信息可在 https://pubs.acs.org/doi/10.1021/jacs.3c05058 免费获得。显示 MY-1B 对 DCAF1_C1113 的立体选择性参与的计算模型；MY-1B核心支架结合策略的计算模型；通过将丙烯酰胺转换为丁炔酰胺来取消 DCAF1 的参与；DCAF1 定向亲电 PROTAC 对 FKBP12 的浓度依赖性和时间依赖性降解；DCAF1 定向亲电 PROTAC 降解重组表达的 HA-FKBP12、内源性 FKBP12 和内源性 BRD4；比较 YT117R 和 YT47R 对 DCAF1 的参与；通过可逆小分子 CYCA-117-70 在 C1113 附近结合 DCAF1；在经 YT47 处理的 HEK293T 细胞中显示大量显着变化的蛋白质列表；生物材料和方法；全凝胶和蛋白质印迹；和合成化学（已更正）(PDF) 大多数电子支持信息文件无需订阅 ACS 网络版即可获得。此类文件可以按文章下载以供研究使用（如果相关文章有链接的公共使用许可，则该许可可能允许其他用途）。可以通过 RightsLink 许可系统请求从 ACS 获得用于其他用途的许可：http://pubs.acs.org/page/copyright/permissions.html。