In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

Context: In our initial attempt to identify differentiation markers for ocular surface epithelia, we observed a unique staining pattern by a commercial anti-Galphaq antibody. We further isolate and characterize the protein reactive with this anti-Galphaq antibody in human ocular surface epithelia.', 'Human donor corneoscleral buttons were sectioned and stained with a battery of commercial antibodies against Galpha proteins. Western blot analysis of cell lysates of corneal epithelial cells and HEK 293 cells transfected with Galphaq cDNA was used to determine the identity of the protein reactive with the anti-Galphaq antibody (E-17). Comparisons were made with another anti-Galphaq antibody (G4415) and an anti-cytokeratin 12C (J7) antibody. The isolated proteins reactive with E17 and J7 were then analyzed with two dimensional isoelectric focusing. Polypeptide sequences were identified using matrix assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF MS) after in-gel protein digestion.', 'The E-17 anti-Galphaq antibody preferentially stained the entire corneal epithelia and the suprabasal layers of the limbus with complete absence of staining in the basal limbus and conjunctiva. Western blot analysis of corneal epithelial cells showed that E-17 antibody identified a protein with a molecular weight of 55 kDa. However, the antibody did not react with the purported antigen, Galphaq protein (42 kDa) produced by Galphaq cDNA. Another anti-Galphaq antibody (G4415) did not react with the 55 kDa protein but did react with the 42 kDa Galphaq protein. Further comparison of the E-17 antibody with the J7 antibody revealed that both recognized the 55 kDa band in one and two dimensional analysis. MALDI-TOF MS analysis confirmed that the 55 kDa protein of interest was actually cytokeratin 12 (CK12), rather than Galphaq protein.\Question: Is cytokeratin 12 in human ocular surface epithelia the antigen reactive with a commercial anti-Galpha q antibody?
The commercial E-17 anti-Galphaq antibody did not react with Galphaq protein, its purported antigen. Instead, it recognized a 55 kDa protein, which was characterized to be cytokeratin 12 by isoelectric focusing and peptide fingerprinting with mass spectrometry. Based on its reactivity with CK12, this commercial E-17 can be used as a differentiation marker to study ocular surface epithelia.

Context: By using the techniques of PCR and restriction fragment length polymorphism (RFLP), we established a classification method for HBV genome based on viral S gene of asymptomatic HBV carriers (AsC).', 'By using this method we classified HBV DNA of AsC living in Guangzhou, Shenyang, Beijing and Chongqing.', 'Among the AsC of Guangzhou, genotype B was 32.8%, genotype C 42.7%, mixed genotypes B and C 23.0%, others 1.6%; among the AsC of Chongqing, genotype B was 35.0%, genotype C 40.0%, mixed genotypes B and C 25.0%; among the AsC of Beijing, genotype B was 25.0%, genotype C 50.0%, mixed genotypes B and C 25.0%; among the AsC of Shenyang, genotype B was 11.1%, genotype C 88.9%. The prevalent HBV strains in China are genotype C and genotype B, and genotype C is the main genotype in west China.\Question: Does [ Establishment of a method for classification of HBV genome and it 's application ]?
The established method for genotyping is simple and convenient. Using this method, we also classified HBV DNA of the patients with chronic hepatitis B and liver cirrhosis living in Guangzhou, and found that mixed genotypes B and C was in 50.0% of the patients detected, suggesting the mixed infection might lead to a severe damage of the liver tissue.

Context: It is unknown whether hypoxia regulates aurora kinase A (AURKA), a serine/threonine kinase, in neuroblastoma to stimulate cell growth or migration. We sought to determine whether AURKA mediates hypoxia-induced regulation of neuroblastoma tumorigenicity.', 'Human neuroblastoma BE(2)-C cells were treated with CoCl2, a chemical hypoxia mimetic, and MLN8237, a pharmalogical inhibitor of AURKA, to assess cell viability, colony formation and transwell migration. Focal adhesion kinase (FAK) expression was analyzed after silencing of AURKA under normoxic vs. hypoxic conditions.', 'Hypoxia up-regulated expression of AURKA mRNA and protein. CoCl2 stimulated cell proliferation and migration, while inhibiting colony formation. MLN8237 reduced colony formation and cell migration. Silencing of AURKA reduced expression of FAK and pFAK under normoxia and hypoxia.\Question: Does targeting aurora kinase A inhibit hypoxia-mediated neuroblastoma cell tumorigenesis?

Hypoxia positively regulates AURKA expression. Hypoxia-induced stimulation of colony formation and migration is, in part, mediated by AURKA. These findings establish that AURKA is a critical regulator of hypoxia-mediated tumor progression in neuroblastoma.