PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
29789366-0	2018	Loss of Upc2p-Inducible ERG3 Transcription Is Sufficient To Confer Niche-Specific Azole Resistance without Compromising Candida albicans Pathogenicity.	Azoles	82-87	potassium voltage-gated channel, subfamily H (eag-related), member 7	Mus musculus	24-28	
29789366-1	2018	Inactivation of sterol Delta5,6-desaturase (Erg3p) in the prevalent fungal pathogen Candida albicans is one of several mechanisms that can confer resistance to the azole antifungal drugs.	Azoles	164-169	potassium voltage-gated channel, subfamily H (eag-related), member 7	Mus musculus	44-49	
29789366-3	2018	This may explain why relatively few erg3-deficient strains have been reported among azole-resistant clinical isolates.	Azoles	84-89	potassium voltage-gated channel, subfamily H (eag-related), member 7	Mus musculus	36-40	
29789366-7	2018	Thus, complete loss of Erg3p activity confers azole resistance but also niche-specific virulence deficiencies.	Azoles	46-51	potassium voltage-gated channel, subfamily H (eag-related), member 7	Mus musculus	23-28	
29789366-8	2018	Serendipitously, we discovered that loss of azole-inducible ERG3 transcription (rather than complete inactivation) is sufficient to confer in vitro fluconazole resistance, without compromising C. albicans stress tolerance, hyphal growth, or pathogenicity in either mouse model.	Azoles	44-49	potassium voltage-gated channel, subfamily H (eag-related), member 7	Mus musculus	60-64	
29789366-10	2018	Collectively, these results establish that modulating Erg3p expression or activity can have niche-specific consequences on both C. albicans pathogenicity and azole resistance.IMPORTANCE While conferring resistance to the azole antifungals in vitro, loss of sterol Delta5,6-desaturase (Erg3p) activity has also been shown to reduce C. albicans pathogenicity.	Azoles	158-163	potassium voltage-gated channel, subfamily H (eag-related), member 7	Mus musculus	54-59	
29789366-10	2018	Collectively, these results establish that modulating Erg3p expression or activity can have niche-specific consequences on both C. albicans pathogenicity and azole resistance.IMPORTANCE While conferring resistance to the azole antifungals in vitro, loss of sterol Delta5,6-desaturase (Erg3p) activity has also been shown to reduce C. albicans pathogenicity.	Azoles	158-163	potassium voltage-gated channel, subfamily H (eag-related), member 7	Mus musculus	285-290	
29789366-10	2018	Collectively, these results establish that modulating Erg3p expression or activity can have niche-specific consequences on both C. albicans pathogenicity and azole resistance.IMPORTANCE While conferring resistance to the azole antifungals in vitro, loss of sterol Delta5,6-desaturase (Erg3p) activity has also been shown to reduce C. albicans pathogenicity.	Azoles	221-226	potassium voltage-gated channel, subfamily H (eag-related), member 7	Mus musculus	54-59	
29789366-10	2018	Collectively, these results establish that modulating Erg3p expression or activity can have niche-specific consequences on both C. albicans pathogenicity and azole resistance.IMPORTANCE While conferring resistance to the azole antifungals in vitro, loss of sterol Delta5,6-desaturase (Erg3p) activity has also been shown to reduce C. albicans pathogenicity.	Azoles	221-226	potassium voltage-gated channel, subfamily H (eag-related), member 7	Mus musculus	285-290	
29789366-13	2018	Most importantly, we have shown that even modest changes in ERG3 transcription are sufficient to confer azole resistance without compromising C. albicans fitness or pathogenicity.	Azoles	104-109	potassium voltage-gated channel, subfamily H (eag-related), member 7	Mus musculus	60-64	
29789366-14	2018	Given that previous efforts to assess the importance of ERG3 as a determinant of clinical azole resistance have focused almost exclusively on detecting null mutants, its role may have been grossly underestimated.	Azoles	90-95	potassium voltage-gated channel, subfamily H (eag-related), member 7	Mus musculus	56-60	
29789366-15	2018	On the basis of our results, a more thorough investigation of the contribution of the ERG3 gene to azole resistance in the clinical setting is warranted.	Azoles	99-104	potassium voltage-gated channel, subfamily H (eag-related), member 7	Mus musculus	86-90	
16436713-4	2006	In this study, we created a C. albicans erg3/erg3 mutant by the "Ura-blaster" method and confirmed the expected azole resistance using standard in vitro testing and the presence of ergosta-7,22-dien-3beta-ol instead of ergosterol.	Azoles	112-117	potassium voltage-gated channel, subfamily H (eag-related), member 7	Mus musculus	40-44	
16436713-4	2006	In this study, we created a C. albicans erg3/erg3 mutant by the "Ura-blaster" method and confirmed the expected azole resistance using standard in vitro testing and the presence of ergosta-7,22-dien-3beta-ol instead of ergosterol.	Azoles	112-117	potassium voltage-gated channel, subfamily H (eag-related), member 7	Mus musculus	45-49	
16127034-11	2005	Reintroduction of a wild-type ERG3 allele into the homozygous deletion mutant restored virulence, ergosterol synthesis, and susceptibility to azoles, confirming that these phenotypic changes were solely due to the inactivation of Erg3p.	Azoles	142-148	potassium voltage-gated channel, subfamily H (eag-related), member 7	Mus musculus	30-34