Updesh Dixit
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View article: FUSE binding protein1 interacts with Tumor Suppressor p53 and p53-Isoforms through their DNA Binding domain: Mapping the FBP1 binding site
FUSE binding protein1 interacts with Tumor Suppressor p53 and p53-Isoforms through their DNA Binding domain: Mapping the FBP1 binding site Open
We have earlier demonstrated that a cellular factor, FUSE binding protein1 (FBP1), physically interacts and effectively suppresses the function of tumor suppressor p53 and promotes persistent HCV replication [Dixit et al. JVI 89:7905, 2015…
View article: Visualization of early RNA replication kinetics of SARS-CoV-2 by using single molecule RNA-FISH
Visualization of early RNA replication kinetics of SARS-CoV-2 by using single molecule RNA-FISH Open
SARS-CoV-2 infection has caused a major global burden. Despite intensive research, the mechanism and dynamics of early viral replication are not completely understood including the kinetics of formation of plus stranded genomic and subgeno…
View article: INI1/SMARCB1 Rpt1 domain mimics TAR RNA in binding to integrase to facilitate HIV-1 replication
INI1/SMARCB1 Rpt1 domain mimics TAR RNA in binding to integrase to facilitate HIV-1 replication Open
INI1/SMARCB1 binds to HIV-1 integrase (IN) through its Rpt1 domain and exhibits multifaceted role in HIV-1 replication. Determining the NMR structure of INI1-Rpt1 and modeling its interaction with the IN-C-terminal domain (IN-CTD) reveal t…
View article: A quantitative single cell, single molecule RNA-FISH+IF and single cell RNA-seq analysis reveals stochasticity of reactivation of latent provirus
A quantitative single cell, single molecule RNA-FISH+IF and single cell RNA-seq analysis reveals stochasticity of reactivation of latent provirus Open
View article: Correction for Dixit et al., “FUSE Binding Protein 1 Facilitates Persistent Hepatitis C Virus Replication in Hepatoma Cells by Regulating Tumor Suppressor p53”
Correction for Dixit et al., “FUSE Binding Protein 1 Facilitates Persistent Hepatitis C Virus Replication in Hepatoma Cells by Regulating Tumor Suppressor p53” Open
View article: Modulation of HCV replication and translation by ErbB3 binding protein1 isoforms
Modulation of HCV replication and translation by ErbB3 binding protein1 isoforms Open
View article: Staufen1 promotes HCV replication by inhibiting protein kinase R and transporting viral RNA to the site of translation and replication in the cells
Staufen1 promotes HCV replication by inhibiting protein kinase R and transporting viral RNA to the site of translation and replication in the cells Open
Persistent hepatitis C virus (HCV) infection leads to chronic hepatitis C (CHC), which often progresses to liver cirrhosis (LC) and hepatocellular carcinoma (HCC). The molecular mechanisms that establish CHC and cause its subsequent develo…
View article: Reciprocal regulation of Abl kinase by Crk Y251 and Abi1 controls invasive phenotypes in glioblastoma
Reciprocal regulation of Abl kinase by Crk Y251 and Abi1 controls invasive phenotypes in glioblastoma Open
Crk is the prototypical member of a class of Src homology 2 (SH2) and Src homology 3 (SH3) domain-containing adaptor proteins that positively regulate cell motility via the activation of Rac1 and, in certain tumor types such as GBM, can pr…
View article: FUSE Binding Protein 1 Facilitates Persistent Hepatitis C Virus Replication in Hepatoma Cells by Regulating Tumor Suppressor p53
FUSE Binding Protein 1 Facilitates Persistent Hepatitis C Virus Replication in Hepatoma Cells by Regulating Tumor Suppressor p53 Open
Hepatitis C virus (HCV) is a leading cause of chronic hepatitis C (CHC), liver cirrhosis, and hepatocellular carcinoma (HCC). Immunohistochemistry of archived HCC tumors showed abundant FBP1 expression in HCC tumors with the CHC background…