Search Results - "Mehta, Kavi P"

Human Papillomaviruses Recruit Cellular DNA Repair and Homologous Recombination Factors to Viral Replication Centers by GILLESPIE, Kenric A, MEHTA, Kavi P, LAIMINS, Laimonis A, MOODY, Cary A

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Human Papillomavirus E7 Enhances Hypoxia-Inducible Factor 1―Mediated Transcription by Inhibiting Binding of Histone Deacetylases by BODILY, Jason M, MEHTA, Kavi P. M, LAIMINS, Laimonis A

“…Infection by human papillomaviruses (HPV) leads to the formation of benign lesions, warts, and in some cases, cervical cancer. The formation of these lesions…”
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Suppression of STAT-1 Expression by Human Papillomaviruses Is Necessary for Differentiation-Dependent Genome Amplification and Plasmid Maintenance by Hong, Shiyuan, Mehta, Kavi P, Laimins, Laimonis A

“…High-risk human papillomaviruses (HPVs) infect stratified epithelia to establish persistent infections that maintain low-copy-number episomes in infected basal…”
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The E7 Open Reading Frame Acts in cis and in trans To Mediate Differentiation-Dependent Activities in the Human Papillomavirus Type 16 Life Cycle by BODILY, Jason M, MEHTA, Kavi P. M, CRUZ, Linda, MEYERS, Craig, LAIMINS, Laimonis A

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CHK1 phosphorylates PRIMPOL to promote replication stress tolerance by Mehta, Kavi P M, Thada, Vaughn, Zhao, Runxiang, Krishnamoorthy, Archana, Leser, Micheal, Lindsey Rose, Kristie, Cortez, David

“…Replication-coupled DNA repair and damage tolerance mechanisms overcome replication stress challenges and complete DNA synthesis. These pathways include fork…”
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Integrator facilitates RNAPII removal to prevent transcription-replication collisions and genome instability by Bhowmick, Rahul, Mehta, Kavi P.M., Lerdrup, Mads, Cortez, David

“…DNA replication preferentially initiates close to active transcription start sites (TSSs) in the human genome. Transcription proceeds discontinuously with an…”
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HMCES Maintains Genome Integrity by Shielding Abasic Sites in Single-Strand DNA by Mohni, Kareem N., Wessel, Sarah R., Zhao, Runxiang, Wojciechowski, Andrea C., Luzwick, Jessica W., Layden, Hillary, Eichman, Brandt F., Thompson, Petria S., Mehta, Kavi P.M., Cortez, David

“…Abasic sites are one of the most common DNA lesions. All known abasic site repair mechanisms operate only when the damage is in double-stranded DNA. Here, we…”
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HMCES Maintains Replication Fork Progression and Prevents Double-Strand Breaks in Response to APOBEC Deamination and Abasic Site Formation by Mehta, Kavi P.M., Lovejoy, Courtney A., Zhao, Runxiang, Heintzman, Darren R., Cortez, David

“…5-Hydroxymethylcytosine (5hmC) binding, ES-cell-specific (HMCES) crosslinks to apurinic or apyrimidinic (AP, abasic) sites in single-strand DNA (ssDNA). To…”
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Vip1 is a kinase and pyrophosphatase switch that regulates inositol diphosphate signaling by Dollins, D. Eric, Bai, Wenli, Fridy, Peter C., Otto, James C., Neubauer, Julie L., Gattis, Samuel G., Mehta, Kavi P. M., York, John D.

“…Inositol diphosphates (PP-IPs), also known as inositol pyrophosphates, are high-energy cellular signaling codes involved in nutrient and regulatory responses…”
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Topoisomerase II poisons inhibit vertebrate DNA replication through distinct mechanisms by Van Ravenstein, Sabrina X, Mehta, Kavi P, Kavlashvili, Tamar, Byl, Jo Ann W, Zhao, Runxiang, Osheroff, Neil, Cortez, David, Dewar, James M

“…Topoisomerase II (TOP2) unlinks chromosomes during vertebrate DNA replication. TOP2 “poisons” are widely used chemotherapeutics that stabilize TOP2 complexes…”
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Self-reversal facilitates the resolution of HMCES DNA-protein crosslinks in cells by Rua-Fernandez, Jorge, Lovejoy, Courtney A., Mehta, Kavi P.M., Paulin, Katherine A., Toudji, Yasmine T., Giansanti, Celeste, Eichman, Brandt F., Cortez, David

“…Abasic sites are common DNA lesions stalling polymerases and threatening genome stability. When located in single-stranded DNA (ssDNA), they are shielded from…”
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Novel Gammapapillomavirus type in the nasal cavity of a wild red colobus (Piliocolobus tephrosceles) by Weary, Taylor E, Mehta, Kavi P M, Goldberg, Tony L

“…Papillomaviruses (PVs) are double-stranded, circular, epitheliotropic DNA viruses causing benign warts (papillomas) or inducing dysplasia that can progress to…”
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