Prevalence, genotype distribution and mutations of hepatitis B virus and the associated risk factors among pregnant women residing in the northern shores of Persian Gulf, Iran.
Result: T1753A, A1761C, and G1764A mutations caused the conversion of Ile Asn at amino acid 127 (I127N), Lys Gln at amino acid 130 (K130Q), and Val Leu at amino acid 131 (V131L) of the X protein, respectively (S3 Fig).
Association between host TNF-alpha, TGF-beta1, p53 polymorphisms, HBV X gene mutation, HBV viral load and the progression of HBV-associated chronic liver disease in Indonesian patients.
Abstract: Significant differences in viral load were found in HBV-infected patients who had X gene mutations, such as R87W/G, I127L/T/N/S and K130M/V131I mutations (P<0.05).
Result: There were significant differences in viral load levels in HBV-infected patients who had X gene mutations, as well as the R87W/G, I127L/T/N/S and K130M/V131I mutation (P<0.05).
Discussion: H94Y and I127L/T/N/S mutations have been as
HBx mutations promote hepatoma cell migration through the Wnt/beta-catenin signaling pathway.
Introduction: 127 (isoleucine to asparagine/serine/threonine), 130 (lysine to methionine), 131 (valine to isoleucine), and 132 (phenylalanine to tyrosine), which might affect the biological activity of HBx.18, 19 However, the potential role of HBx Combo mutations in hepatocarcinogenesis is largely unknown.
Discussion: substitutions (I127N/K130M/V131I/F132Y) that may lead to aberrant biological activity of HBx.
Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression.
Discussion: Regarding the biological aspects, it was suggested that T1753V lead to the enhancement of transactivation and antiproliferation activity of HBx protein by altering HBx aa 127 (I127T/N/S) and enhancement of virus replication leading to persistent infection and higher frequency of HBV-DNA integration events into the human genome.
Hepatitis B virus core promoter mutations contribute to hepatocarcinogenesis by deregulating SKP2 and its target, p21.
Method: In addition, a combination mutant of I127N/K130M/V131/I/F132Y (abbreviated as Combo mutant) was generated.
Method: To generate HBx mutants that correspond to mutations in the basal core promoter region, site-directed mutagenesis was performed at amino acid positions I127N (T1753A), K130M/V131I (A1762T/G1764A) (abbreviated as TA mutant) and F132Y (T1768A) using a Quikchange kit (Stratagene) according to the manufacturer's protocol.
Discussion: Our results in HepG2 and Huh7cells ind
Hepatitis B virus X mutations occurring naturally associated with clinical severity of liver disease among Korean patients with chronic genotype C infection.
Abstract: All five mutation types (V5M/L, P38S, H94Y, I127T/N, and K130M and V131I) affecting the six codons were found to be related significantly to clinical severity.
Comparison of full length sequences of hepatitis B virus isolates in hepatocellular carcinoma patients and asymptomatic carriers of Korea.
Abstract: Third, mutations (I127T/N, K130M, and V131I) at three codons in the carboxy functional region of X protein were observed in isolates from all three HCC patients.
HBV mutation literature information.
PMID: 
2022
PloS one
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