Given a question and a context passage, generate the answer having the word or phrase from the context passage. Here, the answer should be a shortest continous span from the passage.
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Question: Context: Reactive oxygen species are involved in ovulation. The aim of this study was to examine gonadotropin regulation of antioxidant enzyme sulfiredoxin (Srx) and peroxiredoxin 2 (PRDX2) expressions and modification during the ovulatory process in rats. Administration of antioxidants in vivo reduced ovulation rate and cumulus expansion. LH treatment increased H(2)O(2) levels within 15 min, which, in turn, induced Srx gene expression in cultured preovulatory follicles. Treatment of preovulatory follicles with catalase suppressed the stimulatory effect of LH on Akt phosphorylation. LH- or H(2)O(2)-stimulated Srx mRNA levels were suppressed by inhibitors of antioxidant agents and MAPK kinase. An in vivo injection of equine chorionic gonadotropin-human chorionic gonadotropin (hCG) stimulated Srx mRNA within 1 h in granulosa but not thecal cells of preovulatory follicles. Srx protein levels were stimulated from 3 h post-hCG injection. Immunofluorescence analysis revealed that oocytes expressed the Srx protein. Furthermore, hCG treatment increased Srx expression in mural granulosa, theca and cumulus cells, but the Srx protein was not detected in corpora lutea. Gene expression of PRDX2, identified as an Srx-dependent modified enzyme, was stimulated by gonadotropins. In situ hybridization analysis demonstrated that PRDX2 mRNA was detected in oocytes and theca cells as well as granulosa cells of some antral and preovulatory follicles. High levels of PRDX2 mRNA were detected in corpora lutea. Total levels of PRDX2 protein were not changed by gonadotropins. However, levels of hyperoxidized PRDX2 increased within 2-3 h after the hCG injection. Taken together, gonadotropin stimulation of Srx expression and PRDX2 modification in the ovary suggest the existence of an antioxidant system to maintain H(2)O(2) production and elimination during the periovulatory period. 
 Question: What type of enzyme is peroxiredoxin 2 (PRDX2)?

Answer: antioxidant


Question: Context: After Atahualpa's execution, Pizarro installed Atahualpa's brother, Tupac Huallpa, as a puppet Inca ruler, but he soon died unexpectedly, leaving Manco Inca Yupanqui in power. He began his rule as an ally of the Spanish and was respected in the southern regions of the empire, but there was still much unrest in the north near Quito where Atahualpa's generals were amassing troops. Atahualpa's death meant that there was no hostage left to deter these northern armies from attacking the invaders. Led by Atahualpa's generals Ruminahui, Zope-Zupahua and Quisquis, the native armies were finally defeated, effectively ending any organized rebellion in the north of the empire.:221-223,226 Archaeological evidence of the rebellion incident exists. The remains of about 70 men, women, and adolescents were found in the path of a planned expressway near Lima in 2007. Forensic evidence suggests that the natives were killed by European weapons, probably during the uprising in 1536. Manco Inca initially had good relations with Francisco Pizarro and several other Spanish conquistadors. However, in 1535 he was left in Cuzco under the control of Pizarro's brothers, Juan and Gonzalo, who so mistreated Manco Inca that he ultimately rebelled. Under the pretense of recovering a statue of pure gold in the nearby Yucay valley, Manco was able to escape Cuzco.:235-237 
 Question: Who did Tupac Huallpa succeed as Inca ruler?

Answer: atahualpa


Question: Context: Nucleotide excision repair (NER) is a multistep process capable to remove a variety of DNA distorting lesions from prokaryotic and eukaryotic genomes. In eukaryotic cells, the process requires more than 30 proteins to perform the different steps, i.e. recognition of DNA damage, single strand incisions and excision of the lesion-containing DNA fragment and DNA repair synthesis/ligation. NER can operate via two subpathways: global genome repair (GGR) and a specialized pathway coupled to active transcription (transcription-coupled repair, TCR) and directed to DNA lesions in the transcribed strand of active genes. Both in vivo as well as in cultured cells the fast removal of transcription blocking lesions by TCR is crucial to escape from lethal effects of inhibited transcription inhibition The most delicate step in NER is the recognition of the DNA lesions in their different chromatin context and the mechanism of damage recognition in GGR and TCR is principally different and requires specific proteins. In GGR, the XPC-HR23B is essential for the formation of the incision complex. In TCR the Cockayne syndrome (CS) gene products are key players in the recognition of a stalled RNA polymerase the presumed signaling structure for repair of transcribed strands. In this study, we show that the extent of recovery of UV-inhibited transcription and TCR strictly depends on the amount of CSB protein as well as the amount of DNA damage present in the cell. This indicates that the ratio between DNA damage frequency and CSB protein concentration in the cell is rather critical for acute cellular response, i.e. recovery of inhibited transcription upon DNA damage infliction, and hence cellular survival. 
 Question: Which gene strand is targeted by transcription-coupled repair (TCR)?

Answer:
the transcribed strand