Sneha Khator
This is a likely match — the affiliation was inferred from OpenAlex, ORCID, and web sources but has not been fully confirmed. Treat with appropriate caution.
Researcher
Also affiliated: National Institute of Technology Durgapur (2023–2024); Winthrop Rockefeller Foundation (2026)
Graduate Student Researcher
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Sneha Khator's research focuses on the structural and functional properties of enzymes, particularly in the context of microbial organisms. Her work has investigated how specific mutations within the Cellobiohydrolase (Cel7A) enzyme of *Aspergillus fumigatus* can influence its catalytic activity and thermal stability. One study explored the impact of disulfide bond formation between specific loops (A2 and A4) on enzyme performance, while another examined a T416C-I432C mutation. Khator has also been involved in research exploring the role of the FAM60A protein in cellular signaling pathways, specifically its disruption of Sin3/HDAC control and subsequent promotion of YAP1 activation, a process linked to oncogenesis. Her research network includes collaborators such as Michael Bauer, Mohammad Alinoor Rahman, Bolni Marius Nagalo, and Md. Rafikul Islam from the University of Arkansas for Medical Sciences.
Metrics
- h-index: 1
- Publications: 3
- Citations: 3
Selected Publications
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Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation (2026)
Collaboration Network
Top Collaborators
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
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