John W. Tullai

784 total citations
14 papers, 606 citations indexed

About

John W. Tullai is a scholar working on Molecular Biology, Cancer Research and Cellular and Molecular Neuroscience. According to data from OpenAlex, John W. Tullai has authored 14 papers receiving a total of 606 indexed citations (citations by other indexed papers that have themselves been cited), including 10 papers in Molecular Biology, 5 papers in Cancer Research and 3 papers in Cellular and Molecular Neuroscience. Recurrent topics in John W. Tullai's work include Wnt/β-catenin signaling in development and cancer (4 papers), NF-κB Signaling Pathways (4 papers) and Peptidase Inhibition and Analysis (3 papers). John W. Tullai is often cited by papers focused on Wnt/β-catenin signaling in development and cancer (4 papers), NF-κB Signaling Pathways (4 papers) and Peptidase Inhibition and Analysis (3 papers). John W. Tullai collaborates with scholars based in United States and Brazil. John W. Tullai's co-authors include Geoffrey M. Cooper, Michael Schäffer, Simon Kasif, Marc Glucksman, James L. Roberts, Julie R. Graham, Emer S. Ferro, Corie N. Shrimpton, A. Ian Smith and Philip M. Cummins and has published in prestigious journals such as Journal of Biological Chemistry, PLoS ONE and Brain Research.

In The Last Decade

John W. Tullai

14 papers receiving 604 citations

Peers

John W. Tullai
Naoyuki Takada Japan
Robert C. Hayes United States
Lisa Prichard United States
Jordi Malapeira Spain
Christopher Tudan Canada
Nigel T. Goode United Kingdom
Takashi Sakai Japan
Chie Naruse Japan
Ping Jin China
Vanessa Suckow Germany
Naoyuki Takada Japan
John W. Tullai
Citations per year, relative to John W. Tullai John W. Tullai (= 1×) peers Naoyuki Takada

Countries citing papers authored by John W. Tullai

Since Specialization
Citations

This map shows the geographic impact of John W. Tullai's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by John W. Tullai with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites John W. Tullai more than expected).

Fields of papers citing papers by John W. Tullai

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by John W. Tullai. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by John W. Tullai. The network helps show where John W. Tullai may publish in the future.

Co-authorship network of co-authors of John W. Tullai

This figure shows the co-authorship network connecting the top 25 collaborators of John W. Tullai. A scholar is included among the top collaborators of John W. Tullai based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with John W. Tullai. John W. Tullai is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

14 of 14 papers shown
1.
Tullai, John W., et al.. (2013). Inhibition of GSK‐3 activates CREB transcriptional targets during induction of cardiomyocyte hypertrophy. The FASEB Journal. 27(S1). 1 indexed citations
2.
Tullai, John W., Julie R. Graham, & Geoffrey M. Cooper. (2011). A GSK-3-mediated transcriptional network maintains repression of immediate early genes in quiescent cells. Cell Cycle. 10(18). 3072–3077. 27 indexed citations
3.
Tullai, John W., et al.. (2011). AP-1 Is a Component of the Transcriptional Network Regulated by GSK-3 in Quiescent Cells. PLoS ONE. 6(5). e20150–e20150. 17 indexed citations
4.
Graham, Julie R., John W. Tullai, & Geoffrey M. Cooper. (2009). GSK-3 Represses Growth Factor-inducible Genes by Inhibiting NF-κB in Quiescent Cells. Journal of Biological Chemistry. 285(7). 4472–4480. 30 indexed citations
5.
6.
Tullai, John W., et al.. (2007). Immediate-Early and Delayed Primary Response Genes Are Distinct in Function and Genomic Architecture. Journal of Biological Chemistry. 282(33). 23981–23995. 134 indexed citations
7.
Tullai, John W., et al.. (2007). Glycogen Synthase Kinase-3 Represses Cyclic AMP Response Element-binding Protein (CREB)-targeted Immediate Early Genes in Quiescent Cells. Journal of Biological Chemistry. 282(13). 9482–9491. 67 indexed citations
8.
9.
Tullai, John W., et al.. (2004). Identification of Transcription Factor Binding Sites Upstream of Human Genes Regulated by the Phosphatidylinositol 3-Kinase and MEK/ERK Signaling Pathways. Journal of Biological Chemistry. 279(19). 20167–20177. 80 indexed citations
10.
Tullai, John W., Philip M. Cummins, James L. Roberts, et al.. (2000). The Neuropeptide Processing Enzyme EC 3.4.24.15 Is Modulated by Protein Kinase A Phosphorylation. Journal of Biological Chemistry. 275(47). 36514–36522. 39 indexed citations
11.
Ferro, Emer S., John W. Tullai, Marc Glucksman, & James L. Roberts. (1999). Secretion of Metalloendopeptidase 24.15 (EC 3.4.24.15). DNA and Cell Biology. 18(10). 781–789. 45 indexed citations
12.
Crack, Peter J., T. John Wu, Philip M. Cummins, et al.. (1999). The association of metalloendopeptidase EC 3.4.24.15 at the extracellular surface of the AtT-20 cell plasma membrane. Brain Research. 835(2). 113–124. 55 indexed citations
13.
Li, Ji, John W. Tullai, Wan-hua Amy Yu, & Stephen R. Salton. (1998). Regulated expression during development and following sciatic nerve injury of mRNAs encoding the receptor tyrosine phosphatase HPTPζ/RPTPβ. Molecular Brain Research. 60(1). 77–88. 11 indexed citations
14.
Shrimpton, Corie N., Marc Glucksman, Rebecca A. Lew, et al.. (1997). Thiol Activation of Endopeptidase EC 3.4.24.15. Journal of Biological Chemistry. 272(28). 17395–17399. 63 indexed citations

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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