软件动态胎记技术是实现混淆对抗的软件抄袭检测的有效手段之一.然而,多线程程序中线程交织的不确定性对其造成了不可忽视的影响;极端情况下,传统动态胎记技术甚至会判定同一个程序与其自身不存在抄袭关系.对此,提出从多线程程序在同一...软件动态胎记技术是实现混淆对抗的软件抄袭检测的有效手段之一.然而,多线程程序中线程交织的不确定性对其造成了不可忽视的影响;极端情况下,传统动态胎记技术甚至会判定同一个程序与其自身不存在抄袭关系.对此,提出从多线程程序在同一输入下的多条执行轨迹中进行相似部分的识别,并从中抽象出不易受线程交织影响的行为motifs来实现多线程程序的抄袭检测.该方法捕捉程序的动态执行轨迹,经过轨迹修剪、gram匹配以及扩展和抽象,从中提取motifs胎记建模多线程程序的行为;最终,通过衡量motifs胎记的相似性实现程序间潜在抄袭的判定.在一个包含234个不同版本多线程程序的公共数据集上开展的实验表明,motifs胎记是一种可靠的线程感知胎记方法,不仅可有效对抗当下主流的代码混淆技术,相比现有的2种多线程程序抄袭检测方法TreSB(thread-related system call birthmark)和TOB(thread-oblivious birthmark),也体现出更优秀的检测能力.展开更多
Objective Hepatocyte nuclear factor 4-alpha(HNF4A)is a critical transcription factor in the liver and pancreas.Dysfunctions of HNF4A lead to maturity onset diabetes of the young 1(MODY1).Notably,MODY1 patients with HN...Objective Hepatocyte nuclear factor 4-alpha(HNF4A)is a critical transcription factor in the liver and pancreas.Dysfunctions of HNF4A lead to maturity onset diabetes of the young 1(MODY1).Notably,MODY1 patients with HNF4A pathogenic mutations exhibit decreased responses to arginine and reduced plasma triglyceride levels,but the mechanisms remain unclear.This study aims to investigate the potential target genes transcriptionally regulated by HNF4A and explore its role in these metabolic pathways.Methods A stable 293T cell line expressing the HNF1A reporter was overexpressed with HNF4A.RNA sequencing(RNA-seq)was performed to analyze transcriptional differences.Transcription factor binding site prediction was then conducted to identify HNF4A binding motifs in the promoter regions of relevant target genes.Results RNA-seq results revealed a significant upregulation of transmembrane 4 L six family member 5(TM4SF5)mRNA in HNF4A-overexpressing cells.Transcription factor binding predictions suggested the presence of five potential HNF4A binding motifs in the TM4SF5 promoter.Finally,we confirmed that the DR1 site in the-57 to-48 region of the TM4SF5 promoter is the key binding motif for HNF4A.Conclusion This study identified TM4SF5 as a target gene of HNF4A and determined the key binding motif involved in its regulation.Given the role of TM4SF5 as an arginine sensor in mTOR signaling activation and triglyceride secretion,which closely aligns with phenotypes observed in MODY1 patients,our findings provide novel insights into the possible mechanisms by which HNF4A regulates triglyceride secretion in the liver and arginine-stimulated insulin secretion in the pancreas.展开更多
文摘软件动态胎记技术是实现混淆对抗的软件抄袭检测的有效手段之一.然而,多线程程序中线程交织的不确定性对其造成了不可忽视的影响;极端情况下,传统动态胎记技术甚至会判定同一个程序与其自身不存在抄袭关系.对此,提出从多线程程序在同一输入下的多条执行轨迹中进行相似部分的识别,并从中抽象出不易受线程交织影响的行为motifs来实现多线程程序的抄袭检测.该方法捕捉程序的动态执行轨迹,经过轨迹修剪、gram匹配以及扩展和抽象,从中提取motifs胎记建模多线程程序的行为;最终,通过衡量motifs胎记的相似性实现程序间潜在抄袭的判定.在一个包含234个不同版本多线程程序的公共数据集上开展的实验表明,motifs胎记是一种可靠的线程感知胎记方法,不仅可有效对抗当下主流的代码混淆技术,相比现有的2种多线程程序抄袭检测方法TreSB(thread-related system call birthmark)和TOB(thread-oblivious birthmark),也体现出更优秀的检测能力.
文摘Objective Hepatocyte nuclear factor 4-alpha(HNF4A)is a critical transcription factor in the liver and pancreas.Dysfunctions of HNF4A lead to maturity onset diabetes of the young 1(MODY1).Notably,MODY1 patients with HNF4A pathogenic mutations exhibit decreased responses to arginine and reduced plasma triglyceride levels,but the mechanisms remain unclear.This study aims to investigate the potential target genes transcriptionally regulated by HNF4A and explore its role in these metabolic pathways.Methods A stable 293T cell line expressing the HNF1A reporter was overexpressed with HNF4A.RNA sequencing(RNA-seq)was performed to analyze transcriptional differences.Transcription factor binding site prediction was then conducted to identify HNF4A binding motifs in the promoter regions of relevant target genes.Results RNA-seq results revealed a significant upregulation of transmembrane 4 L six family member 5(TM4SF5)mRNA in HNF4A-overexpressing cells.Transcription factor binding predictions suggested the presence of five potential HNF4A binding motifs in the TM4SF5 promoter.Finally,we confirmed that the DR1 site in the-57 to-48 region of the TM4SF5 promoter is the key binding motif for HNF4A.Conclusion This study identified TM4SF5 as a target gene of HNF4A and determined the key binding motif involved in its regulation.Given the role of TM4SF5 as an arginine sensor in mTOR signaling activation and triglyceride secretion,which closely aligns with phenotypes observed in MODY1 patients,our findings provide novel insights into the possible mechanisms by which HNF4A regulates triglyceride secretion in the liver and arginine-stimulated insulin secretion in the pancreas.
