Match tier
Confirmed
Presence
Current · Arkansas
Last published
2026
Sources
OpenAlex · ORCID
Refreshed
2026-10-05
Biography and Research Information
OverviewAI-generated summary
Sneha Khator's research focuses on the molecular mechanisms underlying fungal enzyme function and cellular signaling pathways. She has investigated modifications to the S–S bridge in the Cellobiohydrolase (Cel7A) enzyme of *Aspergillus fumigatus*, demonstrating how specific mutations can enhance catalytic activity and thermostability. Her work also explores the role of FAM60A in regulating the Hippo signaling pathway, finding that its loss promotes oncogenic YAP1 activation by disrupting Sin3/HDAC control.
Khator has published three papers and has an h-index of 1. She collaborates with researchers at the University of Arkansas for Medical Sciences, including Michael Bauer, Mohammad Alinoor Rahman, Bolni Marius Nagalo, and Md. Rafikul Islam. Her recent activity indicates ongoing research contributions.
Metrics
- h-index: 1
- Publications: 3
- Citations: 3
Positions
-
Post doctoral Fellow 2024–presentUniversity of Arkansas for Medical Sciences Biochemistry & molecular Biology ORCID
Selected Publications
-
Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation (2026)
Collaboration Network
Top Collaborators
Mojnu Miah
Winthrop Rockefeller Foundation
1 shared publication
In database
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Md Nazmul Huda
Winthrop Rockefeller Foundation
1 shared publication
In database
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Md Masudul Islam
Winthrop Rockefeller Foundation
1 shared publication
In database
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Dayebgadoh Gerald
Stowers Institute for Medical Research (US)
1 shared publication
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Akash Saha
Winthrop Rockefeller Foundation
1 shared publication
In database
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Jahangir Alam
University of Arkansas for Medical Sciences
1 shared publication
In database
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Janet L. Thornton
The University of Kansas Cancer Center (US)
1 shared publication
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Allen Gies
Winthrop Rockefeller Foundation
1 shared publication
In database
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Michael A. Bauer
Winthrop Rockefeller Foundation
1 shared publication
In database
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Kimberly Stephens
University of Arkansas for Medical Sciences
1 shared publication
In database
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Bolni M. Nagalo
Winthrop Rockefeller Foundation
1 shared publication
In database
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Mohammad A. Rahman
Winthrop Rockefeller Foundation
1 shared publication
In database
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Michael P. Washburn
The University of Kansas Cancer Center (US)
1 shared publication
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Sayem Miah
Winthrop Rockefeller Foundation
1 shared publication
In database
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
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