PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
32866123-1	2020	Objectives Both CYP24A1 and SLC34A1 gene mutations are responsible for idiopathic infantile hypercalcemia, whereas loss-of-function mutations in CYP24A1 (25-OH-vitamin D-24-hydroxylase) lead to a defect in the inactivation of active 1.25(OH)2D; mutations in SLC34A1 encoding renal sodium phosphate cotransporter NaPi-IIa lead to primary renal phosphate wasting combined with an inappropriate activation of vitamin D.	Phosphates	288-297	cytochrome P450 family 24 subfamily A member 1	Homo sapiens	16-23	
32866123-1	2020	Objectives Both CYP24A1 and SLC34A1 gene mutations are responsible for idiopathic infantile hypercalcemia, whereas loss-of-function mutations in CYP24A1 (25-OH-vitamin D-24-hydroxylase) lead to a defect in the inactivation of active 1.25(OH)2D; mutations in SLC34A1 encoding renal sodium phosphate cotransporter NaPi-IIa lead to primary renal phosphate wasting combined with an inappropriate activation of vitamin D.	Phosphates	288-297	cytochrome P450 family 24 subfamily A member 1	Homo sapiens	145-152	
32866123-1	2020	Objectives Both CYP24A1 and SLC34A1 gene mutations are responsible for idiopathic infantile hypercalcemia, whereas loss-of-function mutations in CYP24A1 (25-OH-vitamin D-24-hydroxylase) lead to a defect in the inactivation of active 1.25(OH)2D; mutations in SLC34A1 encoding renal sodium phosphate cotransporter NaPi-IIa lead to primary renal phosphate wasting combined with an inappropriate activation of vitamin D.	Phosphates	288-297	cytochrome P450 family 24 subfamily A member 1	Homo sapiens	160-184	
34721296-1	2021	Mutations in CYP24A1 (vitamin D 24-hydroxylase) and SLC34A1 (renal phosphate transporter NPT2a) cause autosomal recessive Infantile Hypercalcemia type 1 and 2, illustrating links between vitamin D and phosphate metabolism.	Phosphates	201-210	cytochrome P450 family 24 subfamily A member 1	Homo sapiens	13-20	
28075152-0	2016	CYP24 inhibition as a therapeutic target in FGF23-mediated renal phosphate wasting disorders.	Phosphates	65-74	cytochrome P450 family 24 subfamily A member 1	Homo sapiens	0-5	
26141804-6	2015	We also discuss the emergence of "new" genetic diseases such as mutations in the 24-hydroxylase (CYP24A1) gene inducing neonatal hypercalcemia and nephrocalcinosis: we believe that before prescribing conventional vitamin D supplementation as recommended by the national guidelines, pediatricians should quickly rule out a potential genetic abnormality in phosphate/calcium metabolism (namely a history of lithiasis or hypercalcemia) that would lead to further biological investigations.	Phosphates	355-364	cytochrome P450 family 24 subfamily A member 1	Homo sapiens	97-104	
21610497-7	2011	New data from the uremic rat and humans suggest that dysfunctional vitamin D metabolism is due to changes in CYP24A1 expression caused by phosphate and FGF-23 elevations.	Phosphates	138-147	cytochrome P450 family 24 subfamily A member 1	Homo sapiens	109-116	
21610497-8	2011	SUMMARY: Changes in serum phosphate and FGF-23 levels in the CKD patient increase CYP24A1 expression resulting in decreased vitamin D status.	Phosphates	26-35	cytochrome P450 family 24 subfamily A member 1	Homo sapiens	82-89	
34721296-1	2021	Mutations in CYP24A1 (vitamin D 24-hydroxylase) and SLC34A1 (renal phosphate transporter NPT2a) cause autosomal recessive Infantile Hypercalcemia type 1 and 2, illustrating links between vitamin D and phosphate metabolism.	Phosphates	201-210	cytochrome P450 family 24 subfamily A member 1	Homo sapiens	22-46	
34980721-1	2021	CYP24A1 regulates serum vitamin D (VD) levels by inactivating 25(OH)2D3, which is the precursor of the active form of VD (1alpha,25(OH)2D3), and CYP24A1 expression is controlled by multiple calcemic factors such as 1alpha,25(OH)2D3, calcium, and phosphate.	Phosphates	246-255	cytochrome P450 family 24 subfamily A member 1	Homo sapiens	0-7	
34980721-1	2021	CYP24A1 regulates serum vitamin D (VD) levels by inactivating 25(OH)2D3, which is the precursor of the active form of VD (1alpha,25(OH)2D3), and CYP24A1 expression is controlled by multiple calcemic factors such as 1alpha,25(OH)2D3, calcium, and phosphate.	Phosphates	246-255	cytochrome P450 family 24 subfamily A member 1	Homo sapiens	145-152	
35482362-11	2022	This occurs in response to parathyroid hormone (increases CYP27B1), calcitriol itself (decreases CYP27B1 and increases CYP24A1), calcitonin (increases or decreases CYP24A1 and increases CYP27B1), FGF23 (decreases CYP27B1 and increases CYP24A1) and potentially plasma calcium and phosphate levels themselves (mixed effects).	Phosphates	279-288	cytochrome P450 family 24 subfamily A member 1	Homo sapiens	164-171	
35482362-11	2022	This occurs in response to parathyroid hormone (increases CYP27B1), calcitriol itself (decreases CYP27B1 and increases CYP24A1), calcitonin (increases or decreases CYP24A1 and increases CYP27B1), FGF23 (decreases CYP27B1 and increases CYP24A1) and potentially plasma calcium and phosphate levels themselves (mixed effects).	Phosphates	279-288	cytochrome P450 family 24 subfamily A member 1	Homo sapiens	235-242