PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
11836339-10	2002	Our results shed more light on the structure-function relationship of the CYP17 protein indicating that Phe 93 is crucial for both enzymatic activities.	Phenylalanine	104-107	cytochrome P450 family 17 subfamily A member 1	Homo sapiens	74-79	
12706306-6	2003	The other allele contained nine-base pair deletion, located in exon 8, eliminating codons 487-489 (Asp-Ser-Phe) near the carboxy-terminus of P450c17.	Phenylalanine	107-110	cytochrome P450 family 17 subfamily A member 1	Homo sapiens	141-148	
8855840-6	1996	A genetic study on CYP17 revealed a homozygous deletion of phenylalanine (Phe) codon (TTC) at either amino acid position 53 or 54 in exon 1.	Phenylalanine	59-72	cytochrome P450 family 17 subfamily A member 1	Homo sapiens	19-24	
10856480-7	2000	RESULT(S): Two different mutations were detected on CYP17: One was a deletion of the phenylalanine codon (TTC) at either amino acid 53 or 54 in exon 1, and the other was a missense mutation with the substitution of histidine (CAC) by leucine (CTC) at position 373 in exon 6.	Phenylalanine	85-98	cytochrome P450 family 17 subfamily A member 1	Homo sapiens	52-57	
10620365-10	2000	A chimera containing 301 N-terminal rat P450c17 amino acids and lacking the rat P450c17 phenylalanine 343, had the highest lyase activity.	Phenylalanine	88-101	cytochrome P450 family 17 subfamily A member 1	Homo sapiens	80-87	
8855840-6	1996	A genetic study on CYP17 revealed a homozygous deletion of phenylalanine (Phe) codon (TTC) at either amino acid position 53 or 54 in exon 1.	Phenylalanine	74-77	cytochrome P450 family 17 subfamily A member 1	Homo sapiens	19-24	
8345056-4	1993	Analysis of her P450c17 gene by polymerase chain reaction amplification and sequencing showed a nine-base deletion, eliminating codons 487-489 (Asp-Ser-Phe) near the carboxy-terminus of P450c17.	Phenylalanine	152-155	cytochrome P450 family 17 subfamily A member 1	Homo sapiens	16-23	
2808364-3	1989	The CYP17 gene from an individual having partial combined 17 alpha-hydroxylase/17,20-lyase deficiency has been characterized structurally and the homozygous mutation found to be the deletion of the phenylalanine codon (TTC) at either amino acid position 53 or 54 in exon 1.	Phenylalanine	198-211	cytochrome P450 family 17 subfamily A member 1	Homo sapiens	4-9