User:Tori Templin/Sandbox 1: Difference between revisions

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==Introduction==

Acyl-Coenzyme A Cholesterol Acyltransferase (ACAT), or also known as Sterol ''O''-Acyltransferase (SOAT), is an important enzyme in the body.

Cholesterol esters were ~~discovered~~ in arterial lesions in 1910. Between 1980-1995, the interest in ACAT inhibitors grew, but some of the compounds looked at exhibited toxicity. In 1993, an ACAT gene was successfully cloned. This discovery led to more studies with ACAT and atherosclerosis.

Cholesterol esters were found in arterial lesions in 1910, but the first ACAT activity was discovered in the mid 1900's. This led to the inhibition of ACAT as being looked at as a possible strategy of preventing or treating atherosclerosis. Between 1980-1995, the interest in ACAT inhibitors grew, but some of the compounds looked at exhibited toxicity. As they were looking into the function of the ACAT1 gene, ACAT2 was discovered. In 1993, an ACAT gene was successfully cloned. This discovery led to more studies with ACAT and atherosclerosis. Some of these studies used mice and showed cellular toxicity. ACAT inhibition is still being looked into as a strategy for treatment or prevention of atherosclerosis and related diseases.

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 ==Introduction==
 Acyl-Coenzyme A Cholesterol Acyltransferase (ACAT), or also known as Sterol ''O''-Acyltransferase (SOAT), is an important enzyme in the body.
-Cholesterol esters were discovered in arterial lesions in 1910. Between 1980-1995, the interest in ACAT inhibitors grew, but some of the compounds looked at exhibited toxicity. In 1993, an ACAT gene was successfully cloned. This discovery led to more studies with ACAT and atherosclerosis.
+Cholesterol esters were found in arterial lesions in 1910, but the first ACAT activity was discovered in the mid 1900's. This led to the inhibition of ACAT as being looked at as a possible strategy of preventing or treating atherosclerosis. Between 1980-1995, the interest in ACAT inhibitors grew, but some of the compounds looked at exhibited toxicity. As they were looking into the function of the ACAT1 gene, ACAT2 was discovered. In 1993, an ACAT gene was successfully cloned. This discovery led to more studies with ACAT and atherosclerosis. Some of these studies used mice and showed cellular toxicity. ACAT inhibition is still being looked into as a strategy for treatment or prevention of atherosclerosis and related diseases.
 <ref name=”Farese Jr.”>PMID: 16857957</ref>
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