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. 2006 Aug;55(8):1188–1196. doi: 10.1136/gut.2005.070060

Table 2 Primers used in this study.

Gene Sense primer (5′‐3′) Antisense primer (5′‐3′)
STAT1 GCTATTCACAACCACTCATTCA ACAAGATACAGCCACATAGACA
STAT3α GTCCGTGGAACCATACACAA CAATGGTATTGCTGCAGGTG
STAT3β GTCCGTGGAACCATACACAA ACTGCATCAATGAATGGTGTC
SOCS3 TGCGCCTCAAGACCTTCAGC GATGCGCAGGTTCTTGGTCC
PIAS3 TGCTGGCCGGAACAAGAGTG AGGGGGCAAAGAGAGAAGGG
PIAS1 TCCCACCCAATCTTTGTGTG GCCGCATTTTACCAAGTGGA
IFNAR1 AAACAGTCTGGAAACACGCCTG CGCAGCATAAATGACAAACGG
IFNAR2c CCAAAGTCTTGAATTTTCATAAC TGCCTCAGTATCGCTATCAC
IFNAR2a CCAGGAATCAGAATTTTCATAAC TGCCTCAGTATCGCTATCAC
IFNAR2b TCACAGGTGCAGTCATAATG TGCCTCAGTATCGCTATCAC
β‐actin AGCCTCGCCTTTGCCGA CTGGTGCCTGGGGCG
HCV CCTGTGAGGAACTACTGTCT CTATCAGGCAGTACCACAAG

STAT, signal transducer and activator of transcription; SOCS, suppressor of cytokine signalling; PIAS, protein inhibitor of activated STAT; IFNAR, interferon α/β receptor; HCV, hepatitis C virus.