Difference between revisions of "Part:BBa K1926002:Design"

(→‎Design Notes)
 
(One intermediate revision by the same user not shown)
Line 15: Line 15:
 
(Product: 360)
 
(Product: 360)
  
−
Details are all at the main page.
+
Details are all at the [https://parts.igem.org/Part:BBa_K1926002 main page].
  
 
===Source===
 
===Source===
Line 24: Line 24:
  
 
1. Pei, D.S., et al., Analysis of human Ki-67 gene promoter and identification of the Sp1 binding sites for Ki-67 transcription. Tumour Biol, 2012. 33(1): p. 257-66.
 
1. Pei, D.S., et al., Analysis of human Ki-67 gene promoter and identification of the Sp1 binding sites for Ki-67 transcription. Tumour Biol, 2012. 33(1): p. 257-66.
 +
 +
2. Chen, F., et al., IRF1 suppresses Ki-67 promoter activity through interfering with Sp1 activation. Tumor Biology, 2012. 33(6): p. 2217-2225.
 +
 +
3. Wang, M.-J., et al., p53 regulates Ki-67 promoter activity through p53- and Sp1-dependent manner in HeLa cells. Tumor Biology, 2011. 32(5): p. 905.

Latest revision as of 16:44, 18 October 2016


A cyclic promoter of Ki-67 from human genome


Assembly Compatibility:
  • 10
    COMPATIBLE WITH RFC[10]
  • 12
    COMPATIBLE WITH RFC[12]
  • 21
    INCOMPATIBLE WITH RFC[21]
    Illegal XhoI site found at 425
  • 23
    COMPATIBLE WITH RFC[23]
  • 25
    COMPATIBLE WITH RFC[25]
  • 1000
    INCOMPATIBLE WITH RFC[1000]
    Illegal BsaI site found at 422


Design Notes

We got the sequence from human genome through PCR using the following primers:

pKi67-F: ACCTCTGCCCTCCGCCAGCCG

pKi67-R: ACCCGGTGGCCCTACAGGCTACG

(Product: 360)

Details are all at the main page.

Source

The sequence was retrieved from Addgene.

References

1. Pei, D.S., et al., Analysis of human Ki-67 gene promoter and identification of the Sp1 binding sites for Ki-67 transcription. Tumour Biol, 2012. 33(1): p. 257-66.

2. Chen, F., et al., IRF1 suppresses Ki-67 promoter activity through interfering with Sp1 activation. Tumor Biology, 2012. 33(6): p. 2217-2225.

3. Wang, M.-J., et al., p53 regulates Ki-67 promoter activity through p53- and Sp1-dependent manner in HeLa cells. Tumor Biology, 2011. 32(5): p. 905.