# "*": "https://raw.githubusercontent.com/wefindx/schema/master/method/oo-item.yaml" # "base:title": "0oo - 设计分子以模拟或抑制microRNA,如癌基因和肿瘤抑制基因。" "og:title": "设计分子以模拟或抑制microRNA,如癌基因和肿瘤抑制基因。" "og:description": "## 通过干扰微小RNA与其的附着,通过上调或下调转录后RNA来控制细胞生长。 最近,安德烈·文图拉(Andre Ventura)的[视频](https://www.youtube.com/watch?v=Yuvtrho7ehg)介绍解释说,通过将[microRNA]((https://en.wikipedia.org/wiki/MicroRNA)(含有约20-24个核苷酸的小RNA分子)附着到转录后RNA(信使RNA),发现了一个新的控制层,其表观遗传影响DNA的表达。 )。 通常,细胞具有复杂的细胞分裂调节机制。例如,当我们有一个开放性伤口时,细胞会生长并分裂以固定它,然后在伤口愈合时停止分裂。看起来这个过程是由microRNAs调控的,这些microRNAs几年前才被发现。一些microRNA加速细胞生长(“癌基因”)和一些减慢细胞生长(“肿瘤抑制基因”)。 似乎大多数癌症是microRNA失调的结果(例如,过多的癌基因或过多的肿瘤抑制基因)。 幸运的是,microRNAs是小分子,原则上,设计影响它们与RNA结合或模仿它们的药物应该不难。 因此,安德烈·文图拉的视频中解释的想法是设计模仿或干扰癌基因或/或肿瘤抑制基因的分子。 那么一般的方法是对肿瘤细胞进行测序,看看哪些microRNA很丰富。一些加速细胞分裂(并且通常在一些肿瘤细胞中丰富)的微RNA是已知的,例如致癌基因[miR-19](https://en.wikipedia.org/wiki/Mir-19_microRNA_precursor_family#Breast_Cancer)(其在淋巴瘤中高度表达)或肿瘤抑制基因[p53](https://en.wikipedia.org/wiki/P53)。" "og:image": "https://avatars0.githubusercontent.com/u/28134655" "og:url": "/method/123/" "base:css": "/static/css/bootstrap.min.9c25540d6272.css" "base:extra-css": "/static/css/base.57997aeac1df.css" "base:favicon": "/static/favicon.acaa334f0136.ico" "base:body_class": "" "layout:logo": "/static/0oo.8d2a8bbef612.svg" "layout:index": "/" "layout:menu": "/menu/" "layout:categories": "/intents/" "layout:ideas": "/methods/" "layout:projects": "/projects/" "layout:users": "/users/" "layout:about": "/about/" "layout:help": "/help/" "layout:bug_report": "https://github.com/wefindx/0oo" "layout:login": "/accounts/login/" "layout:light-off": "/darken/?darken=true" "layout:set-multilingual": "/mulang/?mulang=true" "layout:lang": "语言" "layout:set-language-post-action": "/i18n/setlang/" "layout:csrf-token": "KtVo5i4wKdeXzQ9Hn6SZOCKqlyotTmRanxp9vJekS1TKBsSbM6qvCzJEoHQnw38R" "layout:input-next": "/method/123/" "layout:languages": [{"code": "ja", "is-active": "false", "name": "日本語"}, {"code": "lt", "is-active": "false", "name": "Lietuviškai"}, {"code": "zh-hans", "is-active": "true", "name": "简体中文"}, {"code": "en", "is-active": "false", "name": "English"}, {"code": "ru", "is-active": "false", "name": "Русский"}, {"code": "oo", "is-active": "false", "name": "O;o,"}] # "item:parent:intents": [{"url": "/intent/8/", "title": "开发有效且通用的癌症治疗方法"}] "item:title": ".:en:Design molecules to mimic or inhibit micro-RNAs like oncogenes and tumor suppressor genes.:cn:设计分子以模拟或抑制microRNA,如癌基因和肿瘤抑制基因。" "item:summary": "None" "item:voting": 0 "item:voting:add": "/admin/hlog/voting/add/?method=123" "item:voting:csrf_token": "KtVo5i4wKdeXzQ9Hn6SZOCKqlyotTmRanxp9vJekS1TKBsSbM6qvCzJEoHQnw38R" "item:voting:submit-value-option": {"selected": "[-]", "value": "-"} "item:voting:submit-value-option": {"selected": "[+]", "value": "+"} "item:base-administration": false "item:body": | .:en Control cell growth by upregulation or downregulation of post-transcriptional RNA by interferring with attachment of microRNAs to it. -- As well explained on Andre Ventura's [video presentation](https://www.youtube.com/watch?v=Yuvtrho7ehg), recently, a new control layer has been discovered, which epigenetically affects the expression of DNA, by attachment of [microRNA](https://en.wikipedia.org/wiki/MicroRNA) (small RNA molecule containing about 20-24 nucleotides) to post-transcriptional (messenger) RNA. Normally, cells have complex mechanism of regulation of cell division. For example, when we have an open wound, cells grow and divide to fix it, and then stop dividing when the wound had healed. It appears this process is regulated by microRNAs, which had been discovered just a few years ago. Some microRNAs accelerate the cell growth ("oncogenes") and some decelerate cell growth ("tumor suppressor genes"). It seems that most cancers are a result of microRNA deregulation (e.g., too much of oncogenes, or too little of tumor suppressor genes). Luckily, microRNAs are small molecules, and in principle, it should not be hard to design drugs that affect their binding to RNA, or mimic them. So, the idea explained in Andre Ventura's video, is to design molecules that mimic or interfere with oncogenes or and/or tumor suppressor genes. The general approach then, would be to sequence the tumor cells, and look, what microRNAs are abundant. Some of the microRNAs that accelerate cell division (and often are abundant in some tumor cells) are known, e.g., oncogene [miR-19](https://en.wikipedia.org/wiki/Mir-19_microRNA_precursor_family#Breast_Cancer) (which is highly expressed in lymphomas), or tumor suppressor gene [p53](https://en.wikipedia.org/wiki/P53). .:cn ## 通过干扰微小RNA与其的附着,通过上调或下调转录后RNA来控制细胞生长。 最近,安德烈·文图拉(Andre Ventura)的[视频](https://www.youtube.com/watch?v=Yuvtrho7ehg)介绍解释说,通过将[microRNA]((https://en.wikipedia.org/wiki/MicroRNA)(含有约20-24个核苷酸的小RNA分子)附着到转录后RNA(信使RNA),发现了一个新的控制层,其表观遗传影响DNA的表达。 )。 通常,细胞具有复杂的细胞分裂调节机制。例如,当我们有一个开放性伤口时,细胞会生长并分裂以固定它,然后在伤口愈合时停止分裂。看起来这个过程是由microRNAs调控的,这些microRNAs几年前才被发现。一些microRNA加速细胞生长(“癌基因”)和一些减慢细胞生长(“肿瘤抑制基因”)。 似乎大多数癌症是microRNA失调的结果(例如,过多的癌基因或过多的肿瘤抑制基因)。 幸运的是,microRNAs是小分子,原则上,设计影响它们与RNA结合或模仿它们的药物应该不难。 因此,安德烈·文图拉的视频中解释的想法是设计模仿或干扰癌基因或/或肿瘤抑制基因的分子。 那么一般的方法是对肿瘤细胞进行测序,看看哪些microRNA很丰富。一些加速细胞分裂(并且通常在一些肿瘤细胞中丰富)的微RNA是已知的,例如致癌基因[miR-19](https://en.wikipedia.org/wiki/Mir-19_microRNA_precursor_family#Breast_Cancer)(其在淋巴瘤中高度表达)或肿瘤抑制基因[p53](https://en.wikipedia.org/wiki/P53)。 "item:source-date": "" "item:permalink": "/method/123/?l=cn" "item:owner": "Mindey" "item:created": "2015-10-08T12:29:23.489000" "item:ownerlink": "/user/147/Mindey" # "item:link:items": "item:link:add": "/admin/hlog/link/add/?parent=123" "item:project:items": "item:project:add": "/admin/hlog/project/add/?parent=123" "item:comment:add": "/methods/addnote?parent=123" "item:comment:add:csrf_token": "KtVo5i4wKdeXzQ9Hn6SZOCKqlyotTmRanxp9vJekS1TKBsSbM6qvCzJEoHQnw38R" "item:comment:form": |
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