A photo of Ruhikanta Meetei.

Member, Division of Experimental Hematology & Cancer Biology

Associate Professor, UC Department of Pediatrics



Biography & Affiliation


I have been a researcher for more than 25 years and began working at Cincinnati Children’s in 2004. My research interests include Fanconi anemia (FA), Bloom syndrome (BLM) and cancer.

I'm working to uncover the molecular mechanism of both FA and BLM. My research discovered three new FA genes and BLM binding proteins, including FANCB, FANCL and FANCM. I have expertise in FA, chromosome instability, DNA repair and multiprotein complexes.

Our study of FA involves the functional analysis of identified gene products as well as the identification of new FA genes and pathways of signal transduction that regulate DNA damage-induced activation of the core complex of FA. FA provides a model system for studying some of the critical questions fundamental to understanding cancer's general biology. Our lab employs biochemical purification of multiprotein complexes extracted from human cells, ribonucleic acid interference (RNAi), gene KO by Crispr-Cas9 system immunoprecipitations and biochemical assays.

I received the ASH Scholar Award from the American Society of Hematology and my research has been funded by federal grants. My work has been published in many respected journals, such as Nature Genetics, Molecular Cell, Genes & Development, Proteins: Structure, Function, and Bioinformatics, Reproduction, Stem Cell Research, Chromosoma: Biology of the Nucleus, Scientific Reports, Cancer Cell, The Journal of Experimental Medicine and Human Molecular Genetics.

Clinical Interests

Fanconi anemia; chromosome instability; DNA repair; multiprotein complex

Research Interests

Functional analysis of Fanconi anemia gene products; identification of new FA genes and signal transduction pathways that regulate DNA damage induced activation of the FA-core complex; biochemical purification of multiprotein complexes from human cell extracts, immunoprecipitation, RNAi, and biochemical assays; Fanconi anemia as a model system to study some of the important fundamental questions of cancer biology in general.

Academic Affiliation

Associate Professor, UC Department of Pediatrics

Research Divisions

Experimental Hematology and Cancer Biology, Cancer and Blood Diseases


BS: Manipur University, India, 1989.

MS: Manipur University, India, 1992.

PhD: Indian Institute of Science, Bangalore, India, 2000.


FANCD2 is required for the repression of germline transposable elements. Nie, Y; Wilson, AF; DeFalco, T; Meetei, AR; Namekawa, SH; Pang, Q. Reviews of Reproduction. 2020; 159:659-668.

Fancd2-deficient hematopoietic stem and progenitor cells depend on augmented mitochondrial translation for survival and proliferation. Chatla, S; Du, W; Wilson, AF; Meetei, AR; Pang, Q. Stem Cell Research. 2019; 40.

The nuclear DEK interactome supports multi-functionality. Smith, EA; Krumpelbeck, EF; Jegga, AG; Prell, M; Matrka, MM; Kappes, F; Greis, KD; Ali, AM; Meetei, AR; Wells, SI. Proteins: Structure, Function and Genetics. 2018; 86:88-97.

Coordination of the recruitment of the FANCD2 and PALB2 Fanconi anemia proteins by an ubiquitin signaling network. Bick, G; Zhang, F; Meetei, AR; Andreassen, PR. Chromosoma. 2017; 126:417-430.

Fancd2 in vivo interaction network reveals a non-canonical role in mitochondrial function. Zhang, T; Du, W; Wilson, AF; Namekawa, SH; Andreassen, PR; Meetei, AR; Pang, Q. Scientific Reports. 2017; 7.

DEK is required for homologous recombination repair of DNA breaks. Smith, EA; Gole, B; Willis, NA; Soria, R; Starnes, LM; Krumpelbeck, EF; Jegga, AG; Ali, AM; Guo, H; Meetei, AR; et al. Scientific Reports. 2017; 7.