Nathan Lanning

Nathan Lanning
California State University, Los Angeles | CSULA · Department of Biological Sciences

Ph.D.

About

37
Publications
14,158
Reads
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890
Citations
Citations since 2016
21 Research Items
486 Citations
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2016201720182019202020212022020406080
2016201720182019202020212022020406080
Introduction
I investigate the contributions of mitochondrial biology and cellular metabolism to disease. I utilize a synthesis of cell and molecular biology, biochemistry, and systems biology to develop novel methods that will successfully enhance our understanding of these important aspects of disease. These basic functions of cell biology provide an excellent platform for teaching and mentoring students in both the classroom and the laboratory. Website: www.lanninglab.com
Additional affiliations
September 2014 - August 2020
California State University, Los Angeles
Position
  • Professor (Associate)
Description
  • I lead the Laboratory of Mitochondrial Systems Biology and teach various cell and molecular biology courses.
August 2010 - present
Grand Valley State University
Position
  • Professor (Associate)
January 2010 - August 2014
Van Andel Research Institute
Position
  • Postdoctoral Fellowship
Education
September 2004 - December 2009
University of Michigan
Field of study
  • Cellular & Molecular Biology
September 1999 - December 2003
Grand Valley State University
Field of study
  • Biology, Chemistry

Publications

Publications (37)
Article
Full-text available
The adaptor protein SH2B1β participates in regulation of the actin cytoskeleton during processes such as cell migration and differentiation. Here, we identify SH2B1β as a new focal adhesion protein. We provide evidence that SH2B1β is phosphorylated in response to phorbol 12-myristate 13-acetate (PMA)-induced protein kinase C (PKC) activation and sh...
Article
Full-text available
Previous studies have shown that growth hormone (GH) recruits the adapter protein SH2B1β to the GH-activated, GH receptor-associated tyrosine kinase JAK2, implicate SH2B1β in GH-dependent actin cytoskeleton remodeling, and suggest that phosphorylation at serine 161 and 165 in SH2B1β releases SH2B1β from the plasma membrane. Here, we examined the ro...
Article
Full-text available
Altered cellular bioenergetics and mitochondrial function are major features of several diseases, including cancer, diabetes, and neurodegenerative disorders. Given this important link to human health, we sought to define proteins within mitochondria that are critical for maintaining homeostatic ATP levels. We screened an RNAi library targeting >1,...
Article
Full-text available
The complexes of the electron transport chain and ATP synthase comprise the oxidative phosphorylation (OXPHOS) system. The reactions of OXPHOS generate the mitochondrial membrane potential, drive the majority of ATP production in respiring cells, and contribute significantly to cellular reactive oxygen species (ROS). Regulation of OXPHOS is therefo...
Article
Full-text available
The ability to detect and respond to hypoxia within a developing tumor appears to be a common feature amongst most cancers. This hypoxic response has many molecular drivers, but none as widely studied as Hypoxia-Inducible Factor 1 (HIF-1). Recent evidence suggests that HIF-1 biology within lung adenocarcinoma (LUAD) may be associated with expressio...
Article
Full-text available
Background Among breast cancers, the triple-negative breast cancer (TNBC) subtype has the worst prognosis with no approved targeted therapies and only standard chemotherapy as the backbone of systemic therapy. Unique metabolic changes in cancer progression provide innovative therapeutic opportunities. The receptor tyrosine kinases (RTKs) epidermal...
Article
Full-text available
DBF4-dependent kinase (DDK) is a two-subunit kinase required for initiating DNA replication at individual origins and is composed of CDC7 kinase and its regulatory subunit DBF4. Both subunits are highly expressed in many diverse tumor cell lines and primary tumors, and this is correlated with poor prognosis. Inhibiting DDK causes apoptosis of tumor...
Data
Supplementary Figure 1: DDK is overexpressed in tumors and is a predictor of poor survival. (A) DDK subunits are significantly overexpressed in lung adenocarcinoma tissue when compared to matched normal tissue. Significance was calculated using Kolmogorov-Smirnov test. (B) CDC7 expression is independently prognostic within the TCGA LUAD cohort (all...
Data
DDK Gene Expression Analysis Using TCGA Lung Adenocarcinoma Data.
Data
Primary RNAi Screen Data Including the Kinase and Phosphatase RNAi Libraries.
Data
Network Analysis of Top 29 Hits from RNAi Screen.
Article
The notoriously high glucose uptake by metastatic melanoma (MM) lesions is commonly exploited clinically using PET/CT imaging to evaluate disease progression and treatment. The purpose of this study was to use patient-derived xenograft (PDX) MM models and a PDX derived (MM8.1) cell line, to determine how driver oncogene mutations and drugs targetin...
Article
Full-text available
We previously performed an RNA interference (RNAi) screen and found that the knockdown of the catalytically inactive phosphatase, MK-STYX [MAPK (mitogen-activated protein kinase) phospho-serine/threonine/tyrosine-binding protein], resulted in potent chemoresistance. Our follow-up studies demonstrated that knockdown of MK-STYX prevents cells from un...
Article
Full-text available
Protein Tyrosine Phosphatase localized to the Mitochondrion 1 (PTPMT1) is a dual specificity phosphatase exclusively localized to the mitochondria, and has recently been shown to be a critical component in the cardiolipin biosynthetic pathway. The downregulation of PTPMT1 in pancreatic beta cells has been shown to increase cellular ATP levels and i...
Article
Full-text available
Mitochondrial processes play an important role in tumor initiation and progression. In this review, we focus on three critical processes by which mitochondrial function may contribute to cancer: through alterations in glucose metabolism, the production of reactive oxygen species (ROS) and compromise of intrinsic apoptotic function. Alterations in c...
Article
Full-text available
Evasion of apoptosis is a significant problem affecting an array of cancers. In order to identify novel regulators of apoptosis, we performed an RNA interference (RNAi) screen against all kinases and phosphatases in the human genome. We identified MK-STYX (STYXL1), a catalytically inactive phosphatase with homology to the mitogen-activated protein...
Article
Full-text available
Regulation of c-Fos transcription by GH is mediated by CCAAT/enhancer binding protein β (C/EBPβ). This study examines the role of C/EBPβ in mediating GH activation of other early response genes, including Cyr61, Btg2, Socs3, Zfp36, and Socs1. C/EBPβ depletion using short hairpin RNA impaired responsiveness of these genes to GH, as seen for c-Fos. R...
Article
Growth hormone (GH) regulates overall body growth and metabolism and is used therapeutically for a variety of clinical applications. GH binding to its receptor activates the tyrosine kinase, JAK2. Active JAK2 initiates multiple cellular responses to GH, including regulation of the cytoskeleton, that lead to cellular proliferation, differentiation a...
Article
Full-text available
Janus kinase 2 (JAK2), a tyrosine kinase that associates with the GH receptor and is activated by GH, has been implicated as a key mediator of GH signaling. Several published reports suggest that members of the Src family of tyrosine kinases may also participate in GH signaling. We therefore investigated the extent to which JAK2 and Src family kina...
Article
Full-text available
Growth hormone (GH) is a major regulatory factor for overall body growth as evidenced by the height extremes in people with abnormal circulating GH levels or GH receptor (GHR) disruptions. GH also affects metabolism, cardiac and immune function, mental agility and aging. Currently, GH is being used therapeutically for a variety of clinical conditio...
Article
Full-text available
Degenerative joint disease, also known as osteoarthritis, is the most common joint disorder in human beings. The molecular mechanism underlying this disease is not fully understood. Here, we report that disruption of mitogen-inducible gene 6 (Mig-6) in mice by homologous recombination leads to early onset degenerative joint disease, which is reveal...
Article
Full-text available
Downstream signaling that results from the interaction of hepatocyte growth factor/scatter factor (HGF/SF) with the receptor tyrosine kinase Met plays critical roles in tumor development, progression, and metastasis. This ligand-receptor pair is an attractive target for new diagnostic and therapeutic agents, preclinical development of which require...

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