NucleaRDB: Extraction of mutation data from the literature

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This data was extracted from Medline abstracts and full texts (when available) in an automated manner.

The table below describes different point mutations at a given position and provides links to other documents. The sentence(s) where the point mutations in ANDR_HUMAN at position 182 were found are listed after the table.

Point mutations at position I182 in ANDR_HUMAN

ProteinANDR_HUMAN (P10275)    Gene: AR,DHTR, NR3C    (other point mutations)Swiss-Prot
Cross-reference table
Family page
PositionI182
General numbering (NucleaRDB) -
DomainN-term
Family alignments 3C4 Androgen (AR)
3C Glucocorticoid-like (GR,MR,PR,AR)
3 Estrogen like (ER,ERR,GR,MR,PR,AR)
Other point mutations at the same position Position 163 in 3C4 Androgen (AR) family
Position 128 in 3C Glucocorticoid-like (GR,MR,PR,AR) family
Position 89 in 3 Estrogen like (ER,ERR,GR,MR,PR,AR) family
Reference #1Alen P, Claessens F, Verhoeven G, Rombauts W, Peeters B
Mol Cell Biol 1999 Sep;19(9):6085-97.		Medline
Text sourceHTML and PDF full texts
Point mutationI182A (True positive)
Reference #2Callewaert L, Verrijdt G, Christiaens V, Haelens A, Claessens F
J Biol Chem 2003 Mar 7;278(10):8212-8.		Medline
Text sourceHTML and PDF full texts
Point mutationI182A (True positive)

Relevant sentences

Reference #1 (Alen P et al.): I182A
  • A mutation in the NTD of activation function AF1a (I182A / L183A) , which dramatically impairs the activity of the AR , has no effect on the intrinsic transcriptional activity of the NTD but interferes with the cooperation between the NTD and the LBD

  • To generate the AF1a mutation (I182A / L183A) , the following oligonucleotides were used: 5'-CCTTAAAGACGCCGCGAGCGAGGCC-3' and 5'-GGCCTCGCTCGCGGCGTCTTTAAGG-3'

  • ** , position of the residues mutated in the AF1a mutant (I182A / L183A) ; diamond , position of the H3 mutant (K720A) ; triangle triangle , position of the AF2 mutant (I898A / I899A)

  • We mutated these residues to alanines (I182A / L183A) and looked at the effect of this point mutation on the transcriptional activity of the native receptor , both in the absence and in the presence of cotransfected TIF2

  • Whereas transcription is induced 10-fold by the addition of 1 nM R1881 to the wild-type receptor (Fig. 8 A , bar 1) , the I182A / L183A mutant can only be induced 2-fold (bar 3)

  • (A) COS 7 cells were cotransfected with 250 ng of pMMTV-luc and 25 ng of expression vector for the wild-type hAR or the I182A / L183A mutant , along with 250 ng of either empty pSG5 (bars 1 and 3) or pSG5-TIF2 (bars 2 and 4) and incubated with DCC-treated medium , supplemented with vehicle alone (ethanol) (open bars) or 1 nM R1881 (solid bars)

  • (B) COS cells were transfected with pMMTV-luc (250 ng) , expression vectors for either the wild-type (bars 1 and 3) or the I182A / L183A mutated (bars 2 and 4) NTD-DBD constructs and either empty pSG5 (bars 1 and 2) or pSG5-SRC-1e (bars 3 and 4)

  • (C) COS 7 cells were transfected with 250 ng of pMMTV-luc and 25 ng of expression plasmid for the wild-type DBD-LBD fragment , along with 250 ng of either empty pSG5 (bars 1 and 2) or expression vector for the wild-type hAR NTD (bar 3) or the NTD carrying the I182A / L183A mutation (bar 4)

  • (D) GST pull-down experiments were carried out as for Fig. 4 C with either GST alone or a GST-DBD-LBD fusion protein and the wild-type (lanes 1 to 3) or I182A / L183A mutated (lane 4) hAR NTD

  • To investigate whether the effect of the AF1a mutation might be due to an impaired intrinsic transcription activation function of the hAR NTD or to a loss of stimulation of AF1 by p160 proteins , transfections were performed with NTD-DBD constructs , either carrying or not carrying the I182A / L183A mutation , with or without cotransfection of SRC-1e

  • In the presence of androgen , the wild-type hAR NTD interacts with the GST-DBD-LBD fusion protein (lanes 1 to 3) whereas the NTD carrying the I182A / L183A mutations does not (lane 4)

  • This effect relies on an intact AF1a region , since cotransfection of the p160 coactivators with the I182A / L183A mutated NTD does not result in cooperativity (bars 8 and 10)

  • (A) COS-7 cells (left graph) or CV-1 cells (right graph) were cotransfected with 250 ng of pMMTV-luc , 25 ng of expression vector for the DBD-LBD construct , and 250 ng of expression vector for either the wild-type or I182A / L183A mutated NTD , for TIF2 , or for SRC-1e as indicated

  • To generate the AF1a mutation (I182A / L183A) , the following oligonucleotides were used: 5 -CCTTAAAGACGCCGCGAGCGAGGCC-3 and 5 -GGCCTCGCTCGCGGCGTCTTTAAGG-3

  • , position of the residues mutated in the AF1a mutant (I182A / L183A) ; { , position of the H3 mutant (K720A) ; , , , position of the AF2 mutant (I898A / I899A)

  • 19 , 1999 TRANSCRIPTIONAL ACTIVATION BY THE ANDROGEN RECEPTOR 6091 constructs , either carrying or not carrying the I182A / L183A mutation , with or without cotransfection of SRC-1e

  • (B) COS cells were transfected with pMMTV-luc (250 ng) , expression vectors for either the wild-type (bars 1 and 3) or the I182A / L183A mutated (bars 2 and 4) NTD-DBD constructs and either empty pSG5 (bars 1 and 2) or pSG5-SRC-1e (bars -->and 4)

Reference #2 (Callewaert L et al.): I182A
  • We already reported the involvement of one LXXLL-like motif , 179LKDIL183 (18 ) , the mutation of which (I182A / L183A) impairs the N / C interaction and the activity of the AR

  • For the mutation L435P in the WHTLF motif and the mutation I182A / L183A in the LKDIL motif , no difference on selective versus nonselective elements was seen

  • N / C Interaction in AR-mediated Transactivation already reported the involvement of one LXXLL-like motif , 179LKDIL183 (18) , the mutation of which (I182A / L183A) impairs the N / C interaction and the activity of the AR

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F.Horn (nucleardbcmbi.kun.nl), 21-Apr-2005