Result: Important substitutions in the X gene included I127T, K130M, and V131I whose frequencies in acute infection were 4%, 8% and 12% respectively and in chronic infection were 24.99%, 45.57%, 45.57% respectively.
Deep sequencing of hepatitis B virus basal core promoter and precore mutants in HBeAg-positive chronic hepatitis B patients.
Result: besides classical A1762T/G1764A and G1896A mutants affecting codons 130/131 of X gene (K130M/V131I) and codon 28 of PC gene (W28stop), another 12 SNPs (nt.1719, nt.1726, nt.1727, nt.1730, nt.1752, nt.1753, nt.1768, nt.1800, nt.1803, nt.1804, nt.1805 and nt.1825) also caused amino acid changes.
HBx mutants differentially affect the activation of hypoxia-inducible factor-1alpha in hepatocellular carcinoma.
Abstract: RESULTS: The dual mutations K130M/V131I enhanced the functionality of HBx as they upregulated the expression and transcriptional activity of HIF-1alpha.
Result: As described above, most of HBx point mutants retained the ability to upregulate HIF-1alpha, and especially the dual mutations K130M/V131I enhanced this function.
Result: Dual point mutations K130M/V131I upregulate HIF-1alpha.
Result: Especially, the mutant HA-K130M/V131I-HBx induced the highest expression of them, compared with wild-type HBx and the other five H
Mutation profiling of the hepatitis B virus strains circulating in North Indian population.
Discussion: K130M and V131I are translated due to basal core promoter mutations Adenine to Threonine at nucleotide position 1762 (A1762T) and Guanosine to Adenine at nucleotide position 1764 (G1764A).
Discussion: In our study we have observed K130M, T36A and G50R to be significantly associated with HCC (Table 9).
Hidden secret in hepatitis B viral X protein mutation and hypoxia-inducible factor-1alpha in hepatocarcinoma cancer.
PMID: 25019072
2014
Hepatobiliary surgery and nutrition
Abstract: The C-terminal region of amino acids 119-140 was important for the stability and transactivation, and the point mutations K130M/V131I enhance the functionality of HIF-1alpha, while C-terminal truncation diminish the HIF-1alpha function.
Novel point and combo-mutations in the genome of hepatitis B virus-genotype D: characterization and impact on liver disease progression to hepatocellular carcinoma.
Result: immune epitopes of HBx ORF was significantly altered with progression of CHB to HCC, except the changes in BCP region, which induce mutations in overlapping HBx ORF such as T1753C to I127T, A1762T and G1764A to K130M and V131I.
Table: K130M
Discussion: 116-127) of HBx are frequently altered in HBV-genotype C and B, but no significant sequence heterogeneity was noted in the epitopes of HBV-genotype D, except three mutations I127T ( PMID: 23903686
2013
Brazilian journal of medical and biological research
Discussion: In addition, the C1653T, T1753C, A1762T, and G1764A mutations lead to H94Y, I127T, K130M, and V131I amino acid substitutions in HBx.
Variability in the precore and core promoter regions of HBV strains in Morocco: characterization and impact on liver disease progression.
Discussion: Moreover, T1768A result in aa changes at HBx codon 132 (F132Y), that have been showed to play a synergetic role with K130M and V131I introduced by A1762T/G1764A for leading to carcinogenesis.
Discussion: The A1762T/G1764A double mutation changes two codons in HBx protein (K130M and V131I).
Interaction of mutant hepatitis B X protein with p53 tumor suppressor protein affects both transcription and cell survival.
Abstract: This study examines the differential activities between wild-type Hepatitis B virus X protein (WtHBx) and a mutant HBx (MutHBx), which bears a hotspot mutation at nucleotides 1,762 and 1,764, resulting in a lysine to methionine change at codon 130 and a valine to isoleucine change at codon 131.
Introduction: This observation is of particular interest to our investigation since the A1762T/G1764A double mutation impacts amino acids 130 and 131 of HBx, causing a lysine to methionine change at amino acid 130 and a valine to isoleucine change at amino acid 131.
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.
Result: We also constructed plasmids encoding muta