Title : Nicotine Directly Induces Endoplasmic Reticulum Stress Response in Rat Placental Trophoblast Giant Cells.

Pub. Date : 2016 May

PMID : 26803847






4 Functional Relationships(s)
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1 Nicotine treatment led to dose-dependent increases in the phosphorylation of PERK[Thr981] and eIF2alpha[Ser51], whereas pretreatment with a nicotinic acetylcholine receptor (nAChR) antagonist (mecamylamine hydrochloride) blocked the induction of PERK phosphorylation, verifying the direct involvement of nicotine and nAChR binding. Nicotine cholinergic receptor nicotinic alpha 2 subunit Rattus norvegicus
2 Nicotine treatment led to dose-dependent increases in the phosphorylation of PERK[Thr981] and eIF2alpha[Ser51], whereas pretreatment with a nicotinic acetylcholine receptor (nAChR) antagonist (mecamylamine hydrochloride) blocked the induction of PERK phosphorylation, verifying the direct involvement of nicotine and nAChR binding. Nicotine cholinergic receptor nicotinic alpha 2 subunit Rattus norvegicus
3 Nicotine treatment led to dose-dependent increases in the phosphorylation of PERK[Thr981] and eIF2alpha[Ser51], whereas pretreatment with a nicotinic acetylcholine receptor (nAChR) antagonist (mecamylamine hydrochloride) blocked the induction of PERK phosphorylation, verifying the direct involvement of nicotine and nAChR binding. Nicotine cholinergic receptor nicotinic alpha 2 subunit Rattus norvegicus
4 Nicotine treatment led to dose-dependent increases in the phosphorylation of PERK[Thr981] and eIF2alpha[Ser51], whereas pretreatment with a nicotinic acetylcholine receptor (nAChR) antagonist (mecamylamine hydrochloride) blocked the induction of PERK phosphorylation, verifying the direct involvement of nicotine and nAChR binding. Nicotine cholinergic receptor nicotinic alpha 2 subunit Rattus norvegicus