Difference between revisions of "Part:BBa K5107000"

Revision as of 15:13, 22 September 2024

HRE_minimal

Hormone Response Element (HRE) is the consensus sequence for the binding site of the androgen, glucocorticoid, mineralocorticoid, and progesterone receptors.[1] 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]

@@ Line 3: / Line 3: @@
 <partinfo>BBa_K5107000 short</partinfo>
-Hormone Response Element (HRE) is the consensus sequence for the binding site of the androgen, glucocorticoid, mineralocorticoid, and progesterone receptors. These inverted repeats are responsible for the interaction of the DNA Binding Domain (DBD) of the receptor with the DNA. In the human cells, these nuclear receptors work mainly as transctription activators when the hormone is present in the cytoplasm. There, protein-hormone interactions trigger the translocation of the receptor to the nucleus where the transcription takes place. Because of the absence of the cofactors in the cell free system, these sites are used as operator sites, meaning that the nuclear receptor-hormone complex can bind to these and block the transcription of the upstream promoter.
+Hormone Response Element (HRE) is the consensus sequence for the binding site of the androgen, glucocorticoid, mineralocorticoid, and progesterone receptors.[1]
 <!-- Add more about the biology of this part here
 ===Usage and Biology===
+These inverted repeats are responsible for the interaction of the DNA Binding Domain (DBD) of the receptor with the DNA. In the human cells, these nuclear receptors work mainly as transctription activators when the hormone is present in the cytoplasm.[2] There, protein-hormone interactions trigger the translocation of the receptor to the nucleus where the transcription takes place. Because of the absence of the cofactors in the cell free system, these sites are used as operator sites, meaning that the nuclear receptor-hormone complex can bind to these and block the transcription of the upstream promoter.
 <!-- -->