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Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

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At least 721 records · Page 40
All sourcesNASA NTRSDOE OSTI
DOE OSTI2018

Involvement of FFA1 and FFA4 in the regulation of cellular functions during tumor progression in colon cancer cells

Highlights: • FFAR1 and FFAR4 expressions are changed by anticancer drugs in colon cancer cells. • FFA1 stimulates and FFA4 inhibits cellular functions of DLD1 cells. • FFAR1 expression is markedly elevated in highly migratory DLD1 cells. • Cell migration and colony formation of DLD1 cells are suppressed by FFA1 inhibition. • FFA1 and FFA4 regulate cellular functions during tumor progression in DLD1 cells. Free fatty acid receptor 1 (FFA1) and FFA4 mediate a variety of biological responses through binding of medium- and long-chain free fatty acids. The aim of this study was to investigate an involvement of FFA1 and FFA4 in the regulation of cellular functions during tumor progression in colon cancer cells. The long-term fluorouracil (5-FU) and cisplatin (CDDP) treated cells were generated from DLD1 cells (DLD-5FU and DLD-CDDP cells, respectively). FFAR1 expressions were lower in DLD-5FU and DLD-CDDP cells than in DLD1 cells. In contrast, DLD-5FU and DLD-CDDP cells showed the high FFAR4 expressions, compared with DLD1 cells. The cell motile activities of DLD-5FU and DLD-CDDP cells were reduced by GW9508 which is an agonist of FFA1 and FFA4. Moreover, GW1100, an antagonist of FFA1, inhibited the cell motile activities of DLD-5FU and DLD-CDDP cells. To evaluate whether FFA1 and FFA4 regulate the enhancement of cell motility, invasion and colony formation, highly migratory (hmDLD1) cells were established from DLD1 cells. FFAR1 expression was significantly higher in hmDLD1 cells than in DLD1 cells, but no change of FFAR4 expression was observed. The elevated cell motile and invasive activities and colony formation of hmDLD1 cells were suppressed by FFA1 inhibition. These results suggest that FFA1 and FFA4 are involved in the regulation of cellular functions during tumor progression in colon cancer DLD1 cells.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

CDK8 regulates the angiogenesis of pancreatic cancer cells in part via the CDK8-β-catenin-KLF2 signal axis

Highlights: • This is the first study to supply the relationship between CDK8 and angiogenesis in pancreatic cancer cells. • CDK8 could promote angiogenesis in pancreatic cancer. • CDK8 stimulates tumorigenesis and angiogenesis in nude mice models. • CDK8 regulates the angiogenesis of pancreatic cancer cells in part via the CDK8-β-catenin-KLF2 signal axis. • CDK8 regulates KLF2 accumulation in pancreatic cancer cells by regulating β-catenin. CDK8 is associated with the transcriptional Mediator complex and has been shown to regulate several transcription factors implicated in cancer. As a pancreatic cancer oncogene, the role of CDK8 in cancer angiogenesis remains unclear. Here, we investigated the contribution of CDK8 in pancreatic cancer angiogenesis and examined the underlying molecular mechanisms.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

The involvement of regulated in development and DNA damage response 1 (REDD1) in the pathogenesis of intervertebral disc degeneration

Regulated in development and DNA damage response 1 (REDD1) is an evolutionarily conserved, ubiquitous protein that responds to various cell stresses. Studies have proved REDD1 is involved in many diseases, such as osteoarthritis and cancer. The present study aimed to investigate the potential role of REDD1 in the pathogenesis of intervertebral disc degeneration (IDD). Analysis of clinical tissue samples showed REDD1 expression was up-regulated during IDD and was correlated with the grade of disc degeneration. Overexpression of REDD1 in normal human nucleus pulposus (NP) cells resulted in extracellular matrix (ECM) degeneration. Further, we investigated the function of REDD1 using a serum deprivation-induced IDD vitro model and found that REDD1 was up-regulated in a temporal manner. However, hypoxia abolished this increase through down-regulation of NF-κB. Knockdown of REDD1 or NF-κB by si-RNA significantly rescued ECM from degeneration both in normoxia and hypoxia. In addition, NF-κB/REDD1 mediated the protection of hypoxia from serum deprivation-induced apoptosis and autophagy in NP cells. These results suggest that REDD1 might play a pivotal role in IDD pathogenesis, thereby potentially providing a new therapeutic target for IDD treatment.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

RNA binding protein DAZAP1 promotes HCC progression and regulates ferroptosis by interacting with SLC7A11 mRNA

Highlights: • DAZAP1 effectively promotes HCC progression. • DAZAP1 negatively regulates ferroptosis in HCC cells. • DAZAP1 interacts with SLC7A11 mRNA, and positively regulates its stability. RNA-binding proteins (RBPs) closely regulate the whole lifecycle of most RNA molecules, from the very early stage of transcription to RNA decay. Dysregulation of RBPs significantly affects the fate of cancer-related transcripts. Therefore, it is imperative to fully understand the complicated RBP-RNA regulatory networks in malignant diseases and to explore novel therapeutic targets. The RBP DAZAP1 (deleted in azoospermia-associated protein 1), originally identified as an important protein in spermatogenesis, had rarely been studied in the context of carcinogenesis. The role of DAZAP1 in hepatocellular carcinoma (HCC) was unveiled in this study. The relative expression of DAZAP1 was significantly upregulated in HCC and was positively associated with several key malignant characteristics and poor postoperative survival in patients. DAZAP1 knockdown by small interfering RNA markedly inhibited HCC cell proliferation, migration and invasion. Furthermore, DAZAP1 significantly reduced cellular sensitivity to sorafenib (SF), which had been proven to be an inducer of ferroptosis by targeting the system Xc{sup −} (composed of a light chain, xCT/SLC7A11, and a heavy chain, 4F2 heavy chain). At the mechanistic level, DAZAP1 was identified as a potent inhibitor of ferroptosis and an efficient binding partner of SLC7A11 mRNA. Further study revealed that DAZAP1 interacted with the 3′UTR (untranslated region) of SLC7A11 mRNA and positively regulated its stability. In our work, we clarified novel functions of DAZAP1 and preliminarily revealed its underlying mechanism in ferroptosis, which may be conducive to the exploration of biomarkers and therapeutic targets in HCC patients.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

Vimentin loss promotes cancer proliferation through up-regulating Rictor/AKT/β-catenin signaling pathway

Vimentin protein is one of the main cytoskeleton and plays an important role in cell motility and metastasis. Nowadays, vimentin is widely studied as an epithelial-mesenchymal transition (EMT) marker of cancer cells while its involvement in cancer proliferation is poorly understood. In this study, we investigated the participation of vimentin in regulating cancer proliferation by silencing VIM gene in four cancer cell lines. Our results demonstrated that vimentin loss significantly induced cancer cell proliferation both in vitro and in vivo, which has not been reported so far. Mechanistically, knockdown of vimentin expression activated AKT phosphorylation and its downstream β-catenin signaling. Nuclear translocation and transcriptional activity of β-catenin was enhanced after silencing vimentin expression. Furthermore, vimentin loss could prevent Rictor from autophagy-dependent degradation via reducing AMPK-mediated autophagy signaling. AICAR, an AMPK activator, down-regulated Rictor and p-AKT levels while vimentin knockdown could rescue the effects. In vivo, it was also found that Ki67 expression and p-AKT/β-catenin signaling pathway were obviously up-regulated in the tumor tissues in which vimentin was silenced compared to control groups. Taken together, these data showed the novel function of vimentin in regulating cancer proliferation via Rictor/AKT/β-catenin signaling pathway, which suggested that it need more careful consideration before inhibiting metastatic cancers through targeting vimentin.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

Proline hydroxylase domain-containing enzymes regulate calcium levels in cardiomyocytes by TRPA1 ion channel

Highlights: • PHD induces calcium release from cardiomyocytes through ryanodine channel. • PHD activates TRPA1 to induce extracellular calcium ions into the cell and further activate the ryanodine channel. • TRPA1 is involved in the regulation of PHD-Ca2+-AMPK signaling pathway. The proline hydroxylase domain-containing enzymes (PHDs) acts as cellular oxygen sensors, inducing a series of responses to hypoxia, especially during the regulation of metabolism and energy homeostasis. The increase of Ca{sup 2+} in cardiomyocytes, induced by the opening of PHD signaling pathway, is the key initiation signal necessary for the PHD-mediated regulation of the energy metabolism pathway, but the underlying molecular mechanism remains incompletely understood. This study used PHD inhibitors (PHIs) and PHD2-specific RNA interference (PHD2shRNA) to inhibit PHD signals in cardiomyocytes to explore whether transient receptor potential ankyrin 1 (TRPA1) is involved in the regulation of calcium ion influx in the PHD activation pathway associated with to AMP-activated protein kinase (AMPK). The Fluo-3AM probe was used to measure changes in free intracellular calcium ion concentrations, and Western blot analysis was used to detect the levels of phosphorylated (P)-AMPK, TRPA1, and P–Ca{sup 2+}/calmodulin-dependent protein kinase Ⅱ (CaMKⅡ) levels. The PHI-mediated inhibition of PHD resulted in an increase in free Ca{sup 2+} fluorescence in cardiomyocytes, which activated AMPK, TRPA1, and CaMKⅡ. The TRPA1 inhibitor HC030031, the CaMKII inhibitor KN93, and a ryanodine inhibitor (Ryanodine) were all able to inhibit the PHI-induced increase in intracellular Ca{sup 2+} and AMPK activation. Both PHIs and PHD2shRNA were able to effectively activate CaMKII and TRPA1. However, an inositol 1,4,5-triphosphate receptor (IP3R) inhibitor and the protein kinase A (PKA) inhibitor H89 did not significantly inhibit the PHI-induced increase in intracellular Ca{sup 2+} and AMPK activation. These results indicated that PHD might activate the CaMKⅡ pathway through the TRPA1 ion channel, inducing the release of calcium from the sarcoplasmic reticulum through ryanodine receptor 2 (RyR2), activating AMPK to initiate the protective effects of hypoxia in cardiomyocytes.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

MiR-10b-5p inhibits tumorigenesis in gastric cancer xenograft mice model through down-regulating Tiam1

Highlights: • MiR-10b-5p acted as a tumor suppressor in gastric cancer by targeting and down-regulating Tiam1. • Overexpression of miR-10b-5p induced apoptosis of gastric cancer cells. • As a specifically chemically modified miRNA mimics, agomir-10b-5p can accumulate in target cells after overcoming membrane and tissue barriers in vivo. • Agomir-10b-5p could be a potential therapeutic agent for the treatment of gastric cancer. The miR-10b-5p plays an important role in gastric cancer development but its exact effect on gastric cancer development in vivo has not been fully studied. We showed that miR-10b-5p inhibited the proliferation and migration of gastric cancer cells by down-regulating Tiam1 which was up-regulated in both gastric cancer cells and tissues. Gastric cancer xenograft experiment showed that lenti-miR-10b-5p treatment and agomir-10b-5p injection could significantly retard tumor growth and reduce tumor size and induced apoptosis. Therefore, our results elucidate the tumor suppressor role of miR-10b-5p in gastric cancer in which it acts as a negative regulator of Tiam1 and also provide a molecular mechanism for agomir-10b-5p to treat gastric cancer.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

miR-126 regulates angiogenesis in myocardial ischemia by targeting HIF-1α

Promoting angiogenesis by targeting various angiogenic regulators has emerged as a new treatment strategy for myocardial ischemia (MI). MicroRNA-126 (miR-126) has been identified as the main regulator of compensatory angiogenesis; however, its role in MI is unclear. A rat MI model and an EA. hy926 endothelial cell hypoxia model were constructed and it was found that miR-126 was highly expressed in both models. The knockdown of HIF-1α expression in EA. hy926 cells in turn downregulated VEGF and CD34 expression and consequently inhibited angiogenesis. MiR-126 inhibitor inhibited EA. hy926 cell migration and tube formation as well as downregulated VEGF and CD34 expression, and these were reversed by transfection of miR-126 mimics. Rescue tests using miR-126 and HIF-1α demonstrated that miR-126-mediated regulation of angiogenesis was dependent on HIF-1α. In summary, miR-126 regulates the occurrence and progression of angiogenesis during MI via HIF-1α and may be a potential new therapeutic target.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2020

Carbon Limitation Leads to Thermodynamic Regulation of Aerobic Metabolism

Organic matter (OM) metabolism in freshwater ecosystems is a critical source of uncertainty in global biogeochemical cycles, yet the processes regulating aerobic respiration in aquatic environments remain poorly understood. Aerobic respiration is typically predicted through kinetic controls such as organic carbon and oxygen concentrations, while assuming thermodynamic regulation has no influence. The role of OM thermodynamics has been mainly explored under anaerobic conditions; however, recent observations have suggested that thermodynamic properties of OM may influence aerobic respiration rates. Here, we explicitly test OM thermodynamics as a key regulator of aerobic respiration. We pair controlled microcosm experiments with ultrahigh-resolution OM characterization to show that aerobic respiration increases with OM thermodynamic favorability under carbon limitation. We also demonstrate a shift in the regulation of aerobic respiration from OM thermodynamics to nitrogen content when carbon is in excess, highlighting a central role for OM thermodynamics particularly in carbon-limited ecosystems. This illuminates a structural gap in aquatic biogeochemical models by demonstrating that both kinetic and thermodynamic constraints can modulate aerobic respiration. Our work therefore proposes a new conceptual model in which thermodynamic and nutrient limitations dually control aerobic respiration.

54 ENVIRONMENTAL SCIENCES↗
DOE OSTI2025

Harnessing the Power of Machine Learning and Omics to Identify Environmental Regulation on Microbial Functional Composition for Soil C, N, and P Cycling

Microbial enzyme-mediated soil organic matter (SOM) decomposition regulates many key ecosystem functions, such as elemental cycling, soil carbon sequestration, and soil fertility. However, representing microbial processes in Earth system models (ESMs) remains challenging due to a limited understanding of the spatial patterns of diverse microbial functions responsible for soil carbon (C), nitrogen (N), and phosphorus (P) cycling as well as the underlying mechanisms regulating their relative abundances across various environments. We collected published metagenomics data across the continental US (CONUS) to identify hundreds of microbial genes involved in soil C, N, and P cycling and grouped them into eight enzyme functional classes (EFCs). Each EFC represented a group of gene-encoded potential enzymes that decompose similar soil compounds. By integrating the abundances of omics-informed EFCs with the corresponding environmental information, we trained a machine learning (ML) model to identify key edaphic, climate, and vegetation factors regulating the abundances of each EFC. Quantitative analysis of effects of these factors revealed that the spatial distribution of eight EFCs for soil C, N, and P cycling across CONUS reflected potential resource optimization strategies of microbial communities under nutrient limitation, preferential organic-mineral associations, and climatological stresses. This insight, together with the interpreted ML tool and the CONUS-level benchmark for EFCs abundances, paves the way for parameterizing environmental-regulated microbial functional dynamics in biogeochemical models.

machine learning↗
DOE OSTI2026

Reservoir Drought Resilience Under Future Warming Scenarios: Regional Disparities Across Heavily Regulated US Basins

Droughts across the U.S. have imposed substantial challenges to the management of water resources. Reservoir drought, one type of hydrological drought, is characterized by abnormally low reservoir storage levels, reflecting combined impacts of natural water shortages and water management practices. We investigate how reservoir drought signatures, particularly onset, severity, duration, recovery and frequency, may shift under rising temperatures, and how these shifts vary by reservoir typology and degree of regulation. By coupling atmosphere-land-river models with reservoir operations at ~12-km resolution, we simulated reservoir storage and characterized reservoir droughts across five heavily regulated U.S. basins. Our findings reveal significant regional and functional disparities in reservoir drought resilience under the scenario of rising temperatures. Reservoirs in the Texas-Gulf region are projected to become more resilient, while systems in the Upper Colorado and South Atlantic-Gulf regions face increased risk due to prolonged drought durations and slower recovery. With respect to primary function, reservoirs used for irrigation and hydropower, particularly those with smaller storage capacity and lower degrees of regulation, are most susceptible to future drought stress. These results are valuable in understanding water availability in highly regulated environments, and the influence of hydrometeorological conditions on storage dynamics. Overall, this study provides the first of its kind benchmark for reservoir droughts at a continental scale to support evolving multi-sectoral drought mitigation efforts. Future research is needed to link reservoir drought conditions to actual supply shortages across competing water uses, while leveraging existing adaptive management strategies and coordinated reservoir operations.

reservoir↗
DOE OSTI2017

Structural basis of dual Ca2+/pH regulation of the endolysosomal TRPML1 channel

The activities of organellar ion channels are often regulated by Ca2+ and H+, which are present in high concentrations in many organelles. Here we report a structural element critical for dual Ca2+/pH regulation of TRPML1, a Ca2+-release channel crucial for endolysosomal function. TRPML1 mutations cause mucolipidosis type IV (MLIV), a severe lysosomal storage disorder characterized by neurodegeneration, mental retardation and blindness. We obtained crystal structures of the 213-residue luminal domain of human TRPML1 containing three missense MLIV-causing mutations. This domain forms a tetramer with a highly electronegative central pore formed by a novel luminal pore loop. Cysteine cross-linking and cryo-EM analyses confirmed that this architecture occurs in the full-length channel. Structure–function studies demonstrated that Ca2+ and H+ interact with the luminal pore and exert physiologically important regulation. The MLIV-causing mutations disrupt the luminal-domain structure and cause TRPML1 mislocalization. Our study reveals the structural underpinnings of TRPML1's regulation, assembly and pathogenesis.

37 INORGANIC, ORGANIC, PHYSICAL, AND ANALYTICAL CH↗
DOE OSTI2018

The MerR-like protein BldC binds DNA direct repeats as cooperative multimers to regulate Streptomyces development

Streptomycetes are notable for their complex life cycle and production of most clinically important antibiotics. A key factor that controls entry into development and the onset of antibiotic production is the 68-residue protein, BldC. BldC is a putative DNA-binding protein related to MerR regulators, but lacks coiled-coil dimerization and effector-binding domains characteristic of classical MerR proteins. Hence, the molecular function of the protein has been unclear. Here we show that BldC is indeed a DNA-binding protein and controls a regulon that includes other key developmental regulators. Intriguingly, BldC DNA-binding sites vary significantly in length. Our BldC-DNA structures explain this DNA-binding capability by revealing that BldC utilizes a DNA-binding mode distinct from MerR and other known regulators, involving asymmetric head-to-tail oligomerization on DNA direct repeats that results in dramatic DNA distortion. Notably, BldC-like proteins radiate throughout eubacteria, establishing BldC as the founding member of a new structural family of regulators.

Science & Technology - Other Topics↗
DOE OSTI2023

Cancer-associated somatic mutations in human phosphofructokinase-1 reveal a critical electrostatic interaction for allosteric regulation of enzyme activity

Metabolic reprogramming, including increased glucose uptake and lactic acid excretion, is a hallmark of cancer. The glycolytic ‘gatekeeper’ enzyme phosphofructokinase-1 (PFK1), which catalyzes the step committing glucose to breakdown, is dysregulated in cancers. While altered PFK1 activity and expression in tumors have been demonstrated, little is known about the effects of cancer-associated somatic mutations. Somatic mutations in PFK1 inform our understanding of allosteric regulation by identifying key amino acid residues involved in the regulation of enzyme activity. Here, we characterized mutations disrupting an evolutionarily conserved salt bridge between aspartic acid and arginine in human platelet (PFKP) and liver (PFKL) isoforms. Using purified recombinant proteins, we showed that disruption of the Asp–Arg pair in two PFK1 isoforms decreased enzyme activity and altered allosteric regulation. We determined the crystal structure of PFK1 to 3.6 Å resolution and used molecular dynamic simulations to understand molecular mechanisms of altered allosteric regulation. We showed that PFKP-D564N had a decreased total system energy and changes in the electrostatic surface potential of the effector site. Cells expressing PFKP-D564N demonstrated a decreased rate of glycolysis, while their ability to induce glycolytic flux under conditions of low cellular energy was enhanced compared with cells expressing wild-type PFKP. Taken together, these results suggest that mutations in Arg–Asp pair at the interface of the catalytic-regulatory domains stabilizes the t-state and presents novel mechanistic insight for therapeutic development in cancer.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2014

Analysis of clock-regulated genes in Neurospora reveals widespread posttranscriptional control of metabolic potential

Significance Circadian clocks regulate gene expression levels to allow an organism to anticipate environmental conditions. These clocks reside in all the major branches of life and confer a competitive advantage to the organisms that maintain them. The clock in the fungus Neurospora crassa is an excellent model for basic understanding of core circadian architecture as well as for filamentous fungi. Here, we identify genes whose expression is clock regulated; indeed, as much as 40% of the transcriptome may be clock regulated, broadly directing daytime catabolism and nighttime growth. Both transcriptional control and posttranscriptional regulation play major roles in control of cycling transcripts such that DNA binding of transcription factors alone appears insufficient to set the phase of circadian transcription.

Hurley, Jennifer M.↗
DOE OSTI2017

LEC1 sequentially regulates the transcription of genes involved in diverse developmental processes during seed development

Significance Seed development is biphasic, consisting of the morphogenesis phase when the basic plant body plan is established and the maturation phase when the embryo accumulates storage reserves and becomes desiccation tolerant. Despite the importance of seeds as human food and animal feed, little is known about the gene-regulatory networks that operate during these phases. We identified genes that are regulated genetically and transcriptionally by a master regulator of seed development, LEAFY COTYLEDON1 (LEC1). We show that LEC1 transcriptionally regulates genes involved in photosynthesis and other developmental processes in early and maturation genes in late seed development. Our results suggest that LEC1 partners with different transcription factors to regulate distinct gene sets and that LEC1 function is conserved in Arabidopsis and soybean seed development.

Pelletier, Julie M.↗
DOE OSTI2021

DNA affinity purification sequencing and transcriptional profiling reveal new aspects of nitrogen regulation in a filamentous fungus

Significance Microorganisms have evolved transcriptional networks to prioritize utilization of available nutrient sources. For filamentous fungi, such as Neurospora crassa , this entails distinguishing between a variety of organic and inorganic nitrogen sources. Here, we transcriptionally profiled the response of N. crassa to a variety of nitrogen sources and used DNA affinity purification sequencing to characterize the role of regulatory genes and their direct downstream targets. We identified a transcription factor responsible for regulating genes involved in amino acid and mannose metabolism. By comparing the genes regulated by transcription factors that regulate specific nitrogen utilization pathways and transcription factors that regulate utilization of all nitrogen sources that require metabolic processing before utilization, we revealed aspects of the nitrogen regulatory network.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2012

DWARF GALAXY FORMATION WITH H{sub 2}-REGULATED STAR FORMATION

We describe cosmological galaxy formation simulations with the adaptive mesh refinement code Enzo that incorporate a star formation prescription regulated by the local abundance of molecular hydrogen. We show that this H{sub 2}-regulated prescription leads to a suppression of star formation in low-mass halos (M{sub h} {approx}< 10{sup 10} M{sub Sun }) at z > 4, alleviating some of the dwarf galaxy problems faced by theoretical galaxy formation models. H{sub 2} regulation modifies the efficiency of star formation of cold gas directly, rather than indirectly reducing the cold gas content with 'supernova feedback'. We determine the local H{sub 2} abundance in our most refined grid cells (76 proper parsec in size at z = 4) by applying the model of Krumholz, McKee, and Tumlinson, which is based on idealized one-dimensional radiative transfer calculations of H{sub 2} formation-dissociation balance in {approx}100 pc atomic-molecular complexes. Our H{sub 2}-regulated simulations are able to reproduce the empirical (albeit lower z) Kennicutt-Schmidt relation, including the low {Sigma}{sub gas} cutoff due to the transition from atomic to molecular phase and the metallicity dependence thereof, without the use of an explicit density threshold in our star formation prescription. We compare the evolution of the luminosity function, stellar mass density, and star formation rate density from our simulations to recent observational determinations of the same at z = 4-8 and find reasonable agreement between the two.

79 ASTRONOMY AND ASTROPHYSICS↗