Hepatitis B virus X protein impedes the DNA repair via its association with transcription factor, TFIIH

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_repair_via_itsassociation_with_transcription_factor_tfiih.html

Hepatitis B virus X protein impedes the DNA repair via its association with

transcription factor, TFIIH

Hepatitis B virus (HBV) infections play an important role in the development of

hepatocellular carcinoma (HCC). HBV X protein (HBx) is a multifunctional protein

that can modulate various cellular processes and plays a crucial role in the

pathogenesis of HCC.

HBx is known to interact with DNA helicase components of TFIIH, a basal

transcriptional factor and an integral component of DNA excision repair.

Results: In this study, the functional relevance of this association was further

investigated in the context to DNA repair. By site-directed mutagenesis HBx's

critical residues for interaction with TFIIH were identified.

Similarly, TFIIH mutants lacking ATPase domain and the conserved

carboxyl-terminal domain failed to interact with HBx. Yeast and mammalian cells

expressing HBxwt conferred hypersensitivity to UV irradiation, which is

interpreted as a basic deficiency in nucleotide excision repair.

HBxmut120 (Glu to Val) was defective in binding to TFIIH and failed to respond

to UV.

Conclusions: We conclude that HBx may act as the promoting factor by inhibiting

DNA repair causing DNA damage and accumulation of errors, thereby contributing

to HCC development.

Author: Ishtiaq QadriKaneez FatimaHany Hafiz

Credits/Source: BMC Microbiology 2011, 11:48

[Guest guest]

http://7thspace.com/headlines/374712/hepatitis_b_virus_x_protein_impedes_the_dna\

_repair_via_itsassociation_with_transcription_factor_tfiih.html

Hepatitis B virus X protein impedes the DNA repair via its association with

transcription factor, TFIIH

Hepatitis B virus (HBV) infections play an important role in the development of

hepatocellular carcinoma (HCC). HBV X protein (HBx) is a multifunctional protein

that can modulate various cellular processes and plays a crucial role in the

pathogenesis of HCC.

HBx is known to interact with DNA helicase components of TFIIH, a basal

transcriptional factor and an integral component of DNA excision repair.

Results: In this study, the functional relevance of this association was further

investigated in the context to DNA repair. By site-directed mutagenesis HBx's

critical residues for interaction with TFIIH were identified.

Similarly, TFIIH mutants lacking ATPase domain and the conserved

carboxyl-terminal domain failed to interact with HBx. Yeast and mammalian cells

expressing HBxwt conferred hypersensitivity to UV irradiation, which is

interpreted as a basic deficiency in nucleotide excision repair.

HBxmut120 (Glu to Val) was defective in binding to TFIIH and failed to respond

to UV.

Conclusions: We conclude that HBx may act as the promoting factor by inhibiting

DNA repair causing DNA damage and accumulation of errors, thereby contributing

to HCC development.

Author: Ishtiaq QadriKaneez FatimaHany Hafiz

Credits/Source: BMC Microbiology 2011, 11:48

[Guest guest]

http://7thspace.com/headlines/374712/hepatitis_b_virus_x_protein_impedes_the_dna\

_repair_via_itsassociation_with_transcription_factor_tfiih.html

Hepatitis B virus X protein impedes the DNA repair via its association with

transcription factor, TFIIH

Hepatitis B virus (HBV) infections play an important role in the development of

hepatocellular carcinoma (HCC). HBV X protein (HBx) is a multifunctional protein

that can modulate various cellular processes and plays a crucial role in the

pathogenesis of HCC.

HBx is known to interact with DNA helicase components of TFIIH, a basal

transcriptional factor and an integral component of DNA excision repair.

Results: In this study, the functional relevance of this association was further

investigated in the context to DNA repair. By site-directed mutagenesis HBx's

critical residues for interaction with TFIIH were identified.

Similarly, TFIIH mutants lacking ATPase domain and the conserved

carboxyl-terminal domain failed to interact with HBx. Yeast and mammalian cells

expressing HBxwt conferred hypersensitivity to UV irradiation, which is

interpreted as a basic deficiency in nucleotide excision repair.

HBxmut120 (Glu to Val) was defective in binding to TFIIH and failed to respond

to UV.

Conclusions: We conclude that HBx may act as the promoting factor by inhibiting

DNA repair causing DNA damage and accumulation of errors, thereby contributing

to HCC development.

Author: Ishtiaq QadriKaneez FatimaHany Hafiz

Credits/Source: BMC Microbiology 2011, 11:48

[Guest guest]

http://7thspace.com/headlines/374712/hepatitis_b_virus_x_protein_impedes_the_dna\

_repair_via_itsassociation_with_transcription_factor_tfiih.html

Hepatitis B virus X protein impedes the DNA repair via its association with

transcription factor, TFIIH

Hepatitis B virus (HBV) infections play an important role in the development of

hepatocellular carcinoma (HCC). HBV X protein (HBx) is a multifunctional protein

that can modulate various cellular processes and plays a crucial role in the

pathogenesis of HCC.

HBx is known to interact with DNA helicase components of TFIIH, a basal

transcriptional factor and an integral component of DNA excision repair.

Results: In this study, the functional relevance of this association was further

investigated in the context to DNA repair. By site-directed mutagenesis HBx's

critical residues for interaction with TFIIH were identified.

Similarly, TFIIH mutants lacking ATPase domain and the conserved

carboxyl-terminal domain failed to interact with HBx. Yeast and mammalian cells

expressing HBxwt conferred hypersensitivity to UV irradiation, which is

interpreted as a basic deficiency in nucleotide excision repair.

HBxmut120 (Glu to Val) was defective in binding to TFIIH and failed to respond

to UV.

Conclusions: We conclude that HBx may act as the promoting factor by inhibiting

DNA repair causing DNA damage and accumulation of errors, thereby contributing

to HCC development.

Author: Ishtiaq QadriKaneez FatimaHany Hafiz

Credits/Source: BMC Microbiology 2011, 11:48