Neil J McKenna, Ph.D.
Associate Professor
Positions
- Associate Professor
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Mol & Cell Biology-O'Malley
Baylor College of Medicine
Houston, TX, US
- Member
-
Dan L Duncan Comprehensive Cancer Center
Baylor College of Medicine
Houston, Texas, United States
Education
- Advanced Training from Baylor College Of Medicine
- 01/2002 - Houston, TX, United States
- PhD from National University Of Ireland
- 12/1995 - Galway, Ireland
Professional Statement
My career as an informatics team scientist began in 2002, when a total of six NIH ICs funded the Nuclear Receptor Signaling Atlas (NURSA), a consortium of leading investigators in nuclear receptor signaling. The goals of the consortium were to (1) generate discovery-driven datasets using then nascent transcriptomic and proteomic platforms, and (2) to distribute these to the community via the internet. Although such distribution is taken for granted today, at the beginning of the 2000s, such resources did not exist outside of intramural NCBI sites. As a NURSA investigator I led the team that designed and developed the NURSA knowledgebase. NURSA was the first US-based dataset repository, and only the second worldwide, to acquire a digital object identifier (DOI) prefix and mint DOIs as persistent identifiers for its datasets. Now a cornerstone of NIH data sharing principles, DOIs have been widely adopted as persistent dataset identifiers by repositories such as Dryad and Figshare. Finally, as part of NURSA I conceived, developed and edited a MEDLINE-indexed specialist nuclear receptor signaling electronic journal, Nuclear Receptor Signaling.
The NIH BD2K (Big Data 2000) initiative created new models for generating, archiving, sharing and analyzing large datasets by the research community. I played an active founding role in the formulation of NIH BD2K-developed policies that culminated in the current NIH Data Sharing Policy. In addition to a direct role in these NIH programs, I served as an advisor or investigator on numerous community data sharing initiatives, including FORCE11, the Research Data Alliance, the NIH Data Discovery Index (DataMed), the Global Alliance for Genomics and Health, the Network Data Exchange and FAIRsharing.org. I used this experience to advise on data sharing practices for a number of NIH-funded investigator team science consortia, including the Mouse Metabolic Phenotyping Consortium and the Molecular Transducers of Physical Activity Consortium (MoTrPAC). Building on these activities, I am currently a co-investigator in the NIDDK Information Network (DKNET), which is developing AI tools for the NIDDK-funded research community.
I led the expansion of NURSA into the Signaling Pathways Project (SPP) website, developing of a suite of investigator-facing meta-analysis tools that leveraged public datasets to identify mechanisms of regulation of gene expression by a broad spectrum of cellular receptors, enzymes and transcription factors. I also devised strategies to enhance access to archived datasets through linking to associated publications, as well as being a recommended data repository for PLOS, the Endocrine Society and Elsevier. As a continuum, the NURSA and SPP sites are in their 23rd year of continuous NIH support, placing them among the longest-running active NIH community team science resources.
I have recently returned to a more active research role in clinical research and drug development in academia and pharma. The deep experience gleaned from my career as a team scientist has helped me lead development of an analytical platform that uses investigator ‘omics-scale datasets to generate high confidence hypotheses around signaling pathways whose gain or loss of function contributes to the observed pattern of clinical gene expression. Illustrating the direct relevance of team science to patient care, our recent eleven-research institute single cell study on idiopathic pulmonary fibrosis introduced the concept of the therapeutic gap, defined as disease-dysregulated transcriptional programs that are not impacted by approved standard of care drugs.
The NIH BD2K (Big Data 2000) initiative created new models for generating, archiving, sharing and analyzing large datasets by the research community. I played an active founding role in the formulation of NIH BD2K-developed policies that culminated in the current NIH Data Sharing Policy. In addition to a direct role in these NIH programs, I served as an advisor or investigator on numerous community data sharing initiatives, including FORCE11, the Research Data Alliance, the NIH Data Discovery Index (DataMed), the Global Alliance for Genomics and Health, the Network Data Exchange and FAIRsharing.org. I used this experience to advise on data sharing practices for a number of NIH-funded investigator team science consortia, including the Mouse Metabolic Phenotyping Consortium and the Molecular Transducers of Physical Activity Consortium (MoTrPAC). Building on these activities, I am currently a co-investigator in the NIDDK Information Network (DKNET), which is developing AI tools for the NIDDK-funded research community.
I led the expansion of NURSA into the Signaling Pathways Project (SPP) website, developing of a suite of investigator-facing meta-analysis tools that leveraged public datasets to identify mechanisms of regulation of gene expression by a broad spectrum of cellular receptors, enzymes and transcription factors. I also devised strategies to enhance access to archived datasets through linking to associated publications, as well as being a recommended data repository for PLOS, the Endocrine Society and Elsevier. As a continuum, the NURSA and SPP sites are in their 23rd year of continuous NIH support, placing them among the longest-running active NIH community team science resources.
I have recently returned to a more active research role in clinical research and drug development in academia and pharma. The deep experience gleaned from my career as a team scientist has helped me lead development of an analytical platform that uses investigator ‘omics-scale datasets to generate high confidence hypotheses around signaling pathways whose gain or loss of function contributes to the observed pattern of clinical gene expression. Illustrating the direct relevance of team science to patient care, our recent eleven-research institute single cell study on idiopathic pulmonary fibrosis introduced the concept of the therapeutic gap, defined as disease-dysregulated transcriptional programs that are not impacted by approved standard of care drugs.
Websites
Signaling Pathways Project
An integrated 'omics knowledgebase for cellular signaling pathways
Selected Publications
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McKenna NJ, Ochsner SA, Waich A, Cala-Garcia J, Echartrea MER, Grimm S, Poli F, Castillo RC, Zuluaga JD, Poli S, Adams TS, Pineda R, Moss B, Ryter SW, Pillich RT, et al. " Single cell transcriptomics in a treatment-segregated cohort exposes a STAT3-regulated therapeutic gap in idiopathic pulmonary fibrosis " bioRxiv. 2025 ;
Pubmed PMID: 40666833. -
Seasock MJ, Shafiquzzaman M, Ruiz-Echartea ME, Kanchi RS, Tran BT, Simon LM, Meyer MD, Erice PA, Lotlikar SL, Wenlock SC, Ochsner SA, Enright A, Carisey AF, Romero F, Rosas IO, King KY, McKenna NJ, Coarfa C, Rodriguez A. " Let-7 restrains an epigenetic circuit in AT2 cells to prevent fibrogenic intermediates in pulmonary fibrosis " Nat Commun. 2025 ; 16 : 4353.
Pubmed PMID: 40348760. -
Keuls RA, Ochsner SA, O'Neill MB, O'Day DR, Miyauchi A, Campbell KM, Lanners N, Goldstein JA, Yee C, McKenna NJ, Parchem RJ, Parchem JG.. " Single-nucleus transcriptional profiling of the placenta reveals the syncytiotrophoblast stress response to COVID-19 " Am J Obstet Gynecol. 2025 ; 232
Pubmed PMID: 40253079. -
Masschelin PM, Ochsner SA, Hartig SM, McKenna NJ, Cox AR.. " Islet single-cell transcriptomic profiling during obesity-induced beta cell expansion in female mice " iScience. 2025 ; 28
Pubmed PMID: 40104055.
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