N
Nagaraja Tirumuru
Researcher at Ohio State University
Publications - 8
Citations - 358
Nagaraja Tirumuru is an academic researcher from Ohio State University. The author has contributed to research in topics: Gene expression & RNA. The author has an hindex of 5, co-authored 8 publications receiving 262 citations.
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Journal ArticleDOI
N(6)-methyladenosine of HIV-1 RNA regulates viral infection and HIV-1 Gag protein expression.
TL;DR: It is shown that YTHDF1–3 proteins recognize m6A-modified HIV-1 RNA and inhibit HIV- 1 infection in cell lines and primary CD4+ T-cells, and suggests an important role of m 6A modification of HIV-3 RNA in viral infection and HIV-2 protein synthesis.
Journal ArticleDOI
N6-Methyladenosine–binding proteins suppress HIV-1 infectivity and viral production
Wuxun Lu,Nagaraja Tirumuru,Corine St. Gelais,Pratibha C. Koneru,Chang C. Liu,Mamuka Kvaratskhelia,Chuan He,Li Wu +7 more
TL;DR: It is found that Y1–3 protein overexpression in HIV-1 target cells decreases viral genomic RNA (gRNA) levels and inhibits both early and late reverse transcription.
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N6-methyladenosine modification of HIV-1 RNA suppresses type-I interferon induction in differentiated monocytic cells and primary macrophages
Shuliang Chen,Sameer Kumar,Constanza E. Espada,Nagaraja Tirumuru,Michael P. Cahill,Lulu Hu,Chuan He,Chuan He,Li Wu +8 more
TL;DR: This paper showed that m6A modification of HIV-1 RNA suppresses the expression of antiviral cytokine type-I interferon (IFN-I) in differentiated human monocytic cells and primary monocyte-derived macrophages.
Journal ArticleDOI
HIV-1 envelope proteins up-regulate N6-methyladenosine levels of cellular RNA independently of viral replication
Nagaraja Tirumuru,Li Wu +1 more
TL;DR: It is shown that HIV-1 infection of CD4+ primary T-cells or Jurkat cells significantly increases m6A levels of cellular RNA independently of viral replication, and suggests thatAIDS-1 gp120 binding to the CD4 receptor is required for m 6A up-regulation in cells.
Journal ArticleDOI
SAMHD1 modulates in vitro proliferation of acute myeloid leukemia-derived THP-1 cells through the PI3K-Akt-p27 axis.
TL;DR: It is implicate that SAMHD1 can regulate AML cell proliferation via modulation of the PI3K-Akt-p27 signaling axis, and that SAM HD1 may affect tumorigenicity by downregulating inflammation.