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Answer :
Final Answer:
B. AP exonuclease is defective in the animal model of APEX mouse.
Explanation:
The high number of AP (apurinic/apyrimidinic) sites in the DNA of the APEX mouse model suggests a deficiency in repairing these lesions. AP sites are gaps in the DNA where a base is missing, often due to the removal of a damaged base. The enzyme responsible for removing these damaged bases and initiating repair is AP exonuclease.
AP exonuclease, also known as APE1, plays a crucial role in the base excision repair (BER) pathway, which is responsible for fixing DNA damage caused by various factors, including chemical agents. When AP sites accumulate due to a defective AP exonuclease, it can lead to DNA mutations and genomic instability.
Option B is the right answer.
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