INT312739

Context Info Confidence 0.59 First Reported 2010 Last Reported 2010 Negated 0 Speculated 0 Reported most in Body Documents 1 Total Number 2 Disease Relevance 0.22 Pain Relevance 0.50

endoplasmic reticulum (UGT2B17)

UGT2B17 (Homo sapiens)

Pain Link Frequency Relevance Heat diclofenac 2 99.70 cINOD 8 99.36 Bioavailability 2 96.36 Pain 2 50.40

Disease Link Frequency Relevance Heat INFLAMMATION 2 99.08 Renal Disease 36 70.64 Pain 2 50.40 Disease 2 12.80 Proteinuria 4 6.40 Obesity 22 5.00 Injury 16 5.00 Focal Segmental Glomerulosclerosis 10 5.00 Chronic Renal Failure 8 5.00 Pulmonary Disease 8 5.00

Sentences Mentioned In

Key:

Protein

Mutation

Event

Anatomy

Negation

Speculation

Pain term

Disease term

A deficiency of the UGT2B17 enzyme decreases the rate of steroid deactivation and elimination, and owing to this, the bioavailability of steroids may be enhanced to a certain extent.

Negative_regulation (deficiency) of UGT2B17 associated with bioavailability

1) Confidence 0.59 Published 2010 Journal Subst Abuse Treat Prev Policy Section Body Doc Link PMC2877023 Disease Relevance 0.07 Pain Relevance 0.05

Sten et al. discovered that commonly used over-the-counter (OTC) non steroidal anti-inflammatory drugs (NSAIDs) like diclofenac and ibuprofen inhibited the testosterone glucuronidation activity of UGT2B17, UGT2B15 and some other UGTs that have previously shown low but detectable activity [43].

Negative_regulation (inhibited) of UGT2B17 associated with inflammation, cinod and diclofenac

2) Confidence 0.43 Published 2010 Journal Subst Abuse Treat Prev Policy Section Body Doc Link PMC2877023 Disease Relevance 0.15 Pain Relevance 0.46

General Comments

This test has worked.