Difference between revisions of "Part:BBa K2440011"

 
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<partinfo>BBa_K2440011 short</partinfo>
 
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It is the target sequence of let-7a, a modularized DNA part from a set of chemically synthetic oligo DNA library.
  
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<!-- Add more about the biology of this part here
 
 
===Usage and Biology===
 
===Usage and Biology===
  
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MiRNA locker assembled by using this modularized DNA part was able to bind let-7a in an Ago2 dependent manner, that is, knockdown of let-7a was achieved by transfecting cells with miRNA locker.
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Let7 is one of the founding members of the miRNA family. It was first found in C.elegans. There are several human let7 have the same base sequence with C.elegans let7, let7a1 is one in this group. The expression of let7 is barely detectable in embryonic stages, but it increases after differentiation and in mature tissues.<sup>1</sup>
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HRAS, KRAS, and NRAS, these three human RAS genes have several let-7 complementary sites in their Untranslated Regions. It allows let-7 miRNA to control their function. The level of let7 in lung tumor’s cell is much lower than in normal cell. The expression of the RAS proteins was significantly higher in lung tumors, it suggests a possible mechanism for let-7 in cancer.<sup>2</sup>
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Compared with cirrhotic livers, the level of LET7A1 was reduced about 70%in cancered livers. It was also happened in all HCC-derived cell lines examined. It may shows that the low level of the expression of LET7A1 promotes the development of cancer.
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===Sequence and Features===
 
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<span class='h3bb'>Sequence and Features</span>
 
<span class='h3bb'>Sequence and Features</span>
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<partinfo>BBa_K2440011 parameters</partinfo>
 
<partinfo>BBa_K2440011 parameters</partinfo>
 
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==Experimental Validation==
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This part is sequenced as correct after construction.
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==Reference==
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1.The tumor suppressor microRNA let-7 represses the HMGA2 oncogene.Lee YS, Dutta A. Genes Dev. 2007 May 1;21(9):1025-30. Epub 2007 Apr 16.
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2.RAS is regulated by the let-7 microRNA family. Johnson SM, Grosshans H, Shingara J, Byrom M, Jarvis R, Cheng A, Labourier E, Reinert KL, Brown D, Slack FJ. Cell. 2005 Mar 11;120(5):635-47.

Latest revision as of 01:32, 1 November 2017


let-7a target sequence

It is the target sequence of let-7a, a modularized DNA part from a set of chemically synthetic oligo DNA library.

Usage and Biology

MiRNA locker assembled by using this modularized DNA part was able to bind let-7a in an Ago2 dependent manner, that is, knockdown of let-7a was achieved by transfecting cells with miRNA locker.

Let7 is one of the founding members of the miRNA family. It was first found in C.elegans. There are several human let7 have the same base sequence with C.elegans let7, let7a1 is one in this group. The expression of let7 is barely detectable in embryonic stages, but it increases after differentiation and in mature tissues.1

HRAS, KRAS, and NRAS, these three human RAS genes have several let-7 complementary sites in their Untranslated Regions. It allows let-7 miRNA to control their function. The level of let7 in lung tumor’s cell is much lower than in normal cell. The expression of the RAS proteins was significantly higher in lung tumors, it suggests a possible mechanism for let-7 in cancer.2

Compared with cirrhotic livers, the level of LET7A1 was reduced about 70%in cancered livers. It was also happened in all HCC-derived cell lines examined. It may shows that the low level of the expression of LET7A1 promotes the development of cancer.

Sequence and Features

Sequence and Features


Assembly Compatibility:
  • 10
    COMPATIBLE WITH RFC[10]
  • 12
    COMPATIBLE WITH RFC[12]
  • 21
    COMPATIBLE WITH RFC[21]
  • 23
    COMPATIBLE WITH RFC[23]
  • 25
    COMPATIBLE WITH RFC[25]
  • 1000
    COMPATIBLE WITH RFC[1000]


Experimental Validation

This part is sequenced as correct after construction.


Reference

1.The tumor suppressor microRNA let-7 represses the HMGA2 oncogene.Lee YS, Dutta A. Genes Dev. 2007 May 1;21(9):1025-30. Epub 2007 Apr 16.

2.RAS is regulated by the let-7 microRNA family. Johnson SM, Grosshans H, Shingara J, Byrom M, Jarvis R, Cheng A, Labourier E, Reinert KL, Brown D, Slack FJ. Cell. 2005 Mar 11;120(5):635-47.