NucleaRDB: Extraction of mutation data from the literature

2005, NucleaRDB.

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

The table below describes the selected point mutation and provides links to other documents. The sentence(s) where the point mutation L319A was found are listed after the table.

The mutated residues are also indicated in the family sequence alignments and hyperlinked to the corresponding mutation pages.

Point mutation L319A in NR1I3_HUMAN

Point mutation:	L319A
Cited point mutation:	Leu319Ala,Leu319
Domain:	LBD HELIX 10-11
General numbering (NucleaRDB):	1046
Protein:	NR1I3_HUMAN (NR1I3,CA)	Swiss-Prot Cross-reference table Family page
Protein isoforms	2
Other point mutations / same protein	List of mutations in NR1I3_HUMAN
Family alignments	1I3 Constitutive Androstane alpha (CAR1) 1I Vitamin D3-like (VDR,PXR,CAR) 1 Thyroid hormone like (TR,RAR,ROR,PPAR,VDR
Other point mutations / same position	Position 381 in 1I Vitamin D3-like (VDR,PXR,CAR) family Position 370 in 1 Thyroid hormone like (TR,RAR,ROR,PPAR,VDR family
Reference:	The peptide near the C terminus regulates receptor CAR nuclear translocation induced by xenochemicals in mouse liver. Zelko I, Sueyoshi T, Kawamoto T, Moore R, Negishi M Mol Cell Biol 2001 Apr;21(8):2838-46.	Medline
Other point mutations / same article	List
Text source	HTML and PDF full texts
Validation status	True positive

Relevant sentences:

Leu319

Ala mutations of Leu313 , Leu316 , or Leu319 abrogated the translocation of CAR in the livers , while those of Leu312 or Leu315 did not affect the nuclear translocation
Amino acid sequence analysis then revealed a small region of CAR that contains a cluster of Leu residues starting with Leu319 toward the N terminus: L312LGLLAEL319 (Fig. 4 )
Retrospectively , the lack of Leu319 was a major reason that hCAR1-318 was unable to translocate to the nucleus in the CPZ-treated livers

L319A

The hCAR[L312A] and hCAR[L315A] mutants translocated to the nucleus after CPZ treatment as the wild-type CAR did , whereas the mutants hCAR[L313A] , hCAR[L316A] , and hCAR[L319A] abrogated the nuclear translocation capability and remained in the cytoplasm even after CPZ treatment (Fig. 5 )

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