The research report should be a detailed narrative explaining the function, biological processes, and localization of the gene product. Citations should be given for all claims.
You should prioritize authoritative reviews and primary scientific literature when conducting research. You can supplement
this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.
We are specifically interested in the primary function of the gene - for enzymes, what reaction is catalyzed, and what is the substrate specificity? For transporters, what is the substrate? For structural proteins or adapters, what is the broader structural role? For signaling molecules, what is the role in the pathway.
We are interested in where in or outside the cell the gene product carries out its function.
We are also interested in the signaling or biochemical pathways in which the gene functions. We are less interested in broad pleiotropic effects, except where these elucidate the precise role.
Include evidence where possible. We are interested in both experimental evidence as well as inference from structure, evolution, or bioinformatic analysis. Precise studies should be prioritized over high-throughput, where available.
The target described in UniProt (O45666) is NHR-49, encoded by nhr-49 (ORF K10C3.6) in Caenorhabditis elegans, and belongs to the nuclear hormone receptor (NHR) family with canonical DNA-binding and ligand-binding domains typical of HNF4/NR2-related receptors. The literature extracted here consistently refers to the C. elegans nuclear hormone receptor NHR-49 with HNF4/PPARα-like roles in lipid metabolism and stress physiology, matching the UniProt-provided identity and domains (Frontiers review 2023-08-14; https://doi.org/10.3389/fphys.2023.1241591) (doering2023nuclearhormonereceptor pages 1-2).
NHR-49 is a sequence-specific transcription factor of the nuclear receptor superfamily. It is widely described as functionally comparable to mammalian lipid-sensing nuclear receptors, especially PPARα (functional analogy) and HNF4α (structural similarity), and is among the best-characterized C. elegans NHRs (review published 2023-08-14; https://doi.org/10.3389/fphys.2023.1241591) (doering2023nuclearhormonereceptor pages 1-2).
Across primary and review sources, the central mechanistic theme is that NHR-49 coordinates transcriptional programs that balance lipid catabolism (β-oxidation), fatty-acid desaturation, lipid remodeling, and stress-protective responses (doering2023nuclearhormonereceptor pages 1-2, pathare2012coordinateregulationof pages 2-3).
A key concept for NHR-49 annotation is context-dependent partnering. In a major genetics study (PLOS Genetics, 2012-04; https://doi.org/10.1371/journal.pgen.1002645), NHR-49 was shown to regulate distinct gene subsets via partnerships with other NHRs, notably:
- NHR-80: linked to regulation of fatty-acid desaturase genes.
- NHR-66: linked to regulation of sphingolipid/lipid remodeling genes.
The same study used NHR-49’s ligand-binding domain (LBD) as bait in yeast two-hybrid screens and reported recovery of multiple candidate interacting factors (pathare2012coordinateregulationof pages 2-3, pathare2012coordinateregulationof pages 14-15).
Primary function: NHR-49 acts as a transcriptional regulator that can both activate and repress metabolic gene programs.
- It activates gene modules involved in fatty-acid β-oxidation (including canonical targets such as acs-2, cpt-5, ech-1) and regulates fatty-acid desaturation genes (fat-5, fat-6, fat-7) (pathare2012coordinateregulationof pages 2-3).
- It is also implicated in stress-protective transcription, including oxidative-stress detoxification programs and regulation of detox genes (e.g., gst-4 in stress contexts) (G3, 2018-12; https://doi.org/10.1534/g3.118.200727) (hu2018thecaenorhabditiselegans pages 1-5).
Coactivator dependence: Multiple studies converge on MDT-15 (Mediator subunit) as a critical co-regulator for NHR-49-driven transcriptional outputs in metabolism and stress programs (hu2018thecaenorhabditiselegans pages 1-5, sala2024nuclearreceptorsignaling pages 1-2).
Evidence strongly supports that the LBD is functionally important and likely ligand-responsive, but a definitive endogenous ligand for NHR-49 is not established.
- Gain-of-function missense mutations in the LBD (PLoS ONE, 2016-09-12; https://doi.org/10.1371/journal.pone.0162708) broadly increase NHR-49-regulated gene expression; structural modeling in that paper supports potential interaction with small molecules (lee2016gainoffunctionallelesin pages 1-2).
- A 2024 PLOS Biology paper proposes that palmitic acid functions as a ligand activating “NHR-49/80” to trigger early development under starvation, but the excerpted evidence notes that direct binding was not conclusively verified (kwon2024regulatoroflipid pages 9-11).
Taken together: ligand regulation is plausible and an active area, but functional annotation should phrase ligands as “putative/proposed” unless binding is directly shown.
The most consistent localization evidence is functional, tissue-specific rescue and transgenic expression.
- Neurons (cell-autonomous behavior control): A 2024 Cells paper (2024-06; https://doi.org/10.3390/cells13110978) shows NHR-49 function in specific oxygen-sensing body cavity neurons (URX, AQR, PQR) is sufficient to restore pathogen avoidance behaviors and normalize neuronal calcium kinetics (kwon2024regulatoroflipid pages 1-2, kwon2024regulatoroflipid pages 9-11).
- Intestine (metabolic and proteostasis programs): A 2024 Genes & Development study (2024-05; https://doi.org/10.1101/gad.351829.124) uses intestinal promoters (e.g., gly-19p::nhr-49::gfp) and shows that intestinal NHR-49 activation improves proteostasis outcomes (sala2024nuclearreceptorsignaling pages 7-8).
- Multi-tissue rescue in hypoxia adaptation: eLife 2022 includes tissue-specific constructs (intestine, hypodermis, neurons, muscle) in defining an essential NHR-49 hypoxia pathway (2022-03; https://doi.org/10.7554/elife.67911) (doering2022nuclearhormonereceptor pages 8-11).
In the canonical model, NHR-49 drives expression of fatty-acid utilization genes, including acs-2, cpt-5, ech-1, linking it to β-oxidation and lipid consumption pathways (pathare2012coordinateregulationof pages 2-3).
NHR-49 regulates Δ9-desaturase genes fat-5/fat-6/fat-7, connecting it to MUFA production and lipid composition (pathare2012coordinateregulationof pages 2-3). A 2024 neuronal study further connects altered lipid composition in nhr-49 mutants to altered neuronal activity (kwon2024regulatoroflipid pages 9-11).
Pathare et al. (2012-04; https://doi.org/10.1371/journal.pgen.1002645) is central evidence that NHR-49’s downstream outputs partition into distinct modules depending on partner receptor context (notably NHR-66 and NHR-80), including sphingolipid/lipid remodeling genes (pathare2012coordinateregulationof pages 1-2, pathare2012coordinateregulationof pages 2-3).
NHR-49 is required for induction of detoxification programs (phase II enzymes) in oxidative stress contexts and works with MDT-15; it can also influence SKN-1 isoform expression in this context (G3, 2018-12; https://doi.org/10.1534/g3.118.200727) (hu2018thecaenorhabditiselegans pages 1-5).
A major mechanistic expansion beyond “lipid metabolism” is an essential hypoxia survival pathway controlled by NHR-49 that operates in parallel to HIF-1, with NHR-49 being required for hypoxia-induced autophagosome formation (LGG-1::GFP foci) in seam cells (eLife, 2022-03; https://doi.org/10.7554/elife.67911) (doering2022nuclearhormonereceptor pages 8-11).
A 2024 Genes & Development study places NHR-49/MDT-15 as a signaling module that links lipid metabolic remodeling to HSF-1-dependent heat shock response and proteostasis, demonstrating that NHR-49 activation can be sufficient to improve proteostasis measures (sala2024nuclearreceptorsignaling pages 1-2, sala2024nuclearreceptorsignaling pages 7-8).
A 2024 Cells paper identifies a cell-autonomous neuronal role: loss of nhr-49 causes impaired pathogen lawn avoidance (PA14) associated with prolonged URX calcium transients after O2 upshift, and neuronal rescue in URX/AQR/PQR improves both behavior and calcium kinetics. This work links lipid homeostasis and neuronal excitability and demonstrates a direct neural implementation of nhr-49 function beyond intestinal metabolism (kwon2024regulatoroflipid pages 1-2, kwon2024regulatoroflipid pages 9-11).
Doering et al. (Frontiers in Physiology, 2023-08-14; https://doi.org/10.3389/fphys.2023.1241591) consolidates NHR-49 as a hub integrating lipid metabolism with stress resilience, immunity, and healthy aging, and highlights open questions including tissue-specific outputs and upstream inputs (including ligand-like regulation) (doering2023nuclearhormonereceptor pages 1-2).
Jeong et al. (Nature Communications, 2023-01; https://doi.org/10.1038/s41467-023-35952-z) positions NHR-49 in a whole-animal signaling chain linking glucose restriction → neuronal AMPK signaling → peripheral lipid remodeling, reporting that restoration of NHR-49 in either neurons or intestine can rescue glucose-restriction longevity in an nhr-49 mutant background, consistent with non-cell-autonomous signaling (jeong2023anewampk pages 9-10).
Sala et al. (Genes & Development, 2024-05; https://doi.org/10.1101/gad.351829.124) reports a lipid–proteostasis coupling in which NHR-49/MDT-15 acts upstream of HSF-1, linking reproductive/metabolic cues to organismal stress resilience; it provides quantitative aggregate-reduction data (sala2024nuclearreceptorsignaling pages 7-8).
Kwon et al. (Cells, 2024-06; https://doi.org/10.3390/cells13110978) provides a neuron-specific implementation: NHR-49 in URX/AQR/PQR is required for normal calcium dynamics and PA14 avoidance, and dietary oleic acid can rescue deficits (kwon2024regulatoroflipid pages 1-2, kwon2024regulatoroflipid pages 9-11).
In Sala et al. (2024-05), intestinal activation of NHR-49 reduced polyglutamine aggregation: Q35::mCherry aggregates were reduced by 30% at day 5 of adulthood in an NHR-49-activated condition (sala2024nuclearreceptorsignaling pages 7-8).
Kwon et al. (2024-06) uses multiple quantitative readouts for URX calcium transients (peak amplitude, rise/decay times, AUC, repolarization durations) and reports that 300 µM oleic acid improved avoidance behavior and URX calcium kinetics; imaging trials with maximum ΔF/F0 < 300% were excluded per QC criteria (kwon2024regulatoroflipid pages 2-4, kwon2024regulatoroflipid pages 9-11).
Doering et al. (eLife, 2022-03) reports embryo-to-L4 survival after hypoxia and quantifies autophagy dependence. Example quantitative outcomes include:
- After 24 h at 0.5% O2, approximately 86% of WT embryos reached at least L4; after 48 h, approximately 44% of WT reached L4 (visual evidence in cropped figures) (doering2022nuclearhormonereceptor media de728d3f).
- Autophagy gene perturbations reduced survival, e.g. RNAi of bec-1 to 27% and atg-10 to 28% versus 79% for empty-vector control; multiple autophagy mutants fell in the 41–44% range under hypoxia (doering2022nuclearhormonereceptor pages 8-11).
These data support NHR-49 as a transcriptional regulator upstream of an autophagy module required for hypoxia tolerance (doering2022nuclearhormonereceptor pages 8-11).
Pathare et al. (2012-04) reports microarray significance thresholds used to define NHR-49-regulated genes (absolute log2 ratio ≥ 0.848 and p ≤ 0.001) (pathare2012coordinateregulationof pages 1-2).
Because NHR-49 integrates lipid metabolism with stress resilience and aging, it is widely used as:
- A genetic node to test how interventions (dietary composition, fasting, glucose restriction) reprogram metabolism and stress resistance (doering2023nuclearhormonereceptor pages 1-2, jeong2023anewampk pages 9-10).
- A tissue-specific biology model (neurons vs intestine vs hypodermis) for dissecting cell-autonomous versus systemic lipid signaling mechanisms (kwon2024regulatoroflipid pages 1-2, sala2024nuclearreceptorsignaling pages 7-8, doering2022nuclearhormonereceptor pages 8-11).
Recent primary studies show NHR-49-dependent phenotypes are modifiable by defined nutritional manipulations:
- Oleic acid supplementation (300 µM) modifies neuronal physiology and PA14 avoidance in nhr-49 mutants, operationalizing lipid supplementation as a functional test of NHR-49-linked lipid dysfunction in neurons (kwon2024regulatoroflipid pages 2-4, kwon2024regulatoroflipid pages 9-11).
- In glucose restriction models, NHR-49 sits in a chain connecting dietary inputs to membrane lipid remodeling and longevity, making it a practical target for mechanism-driven dietary/genetic perturbation experiments (jeong2023anewampk pages 9-10).
A consistent expert perspective, especially in the 2023 Frontiers review, is that NHR-49 should be annotated not merely as a “lipid metabolism regulator,” but as a systems integrator that:
1) couples lipid catabolism/desaturation programs to organismal stress-defense networks, and
2) produces tissue-specific outputs (intestinal metabolic remodeling; neuronal excitability control; hypoxia/autophagy survival) while potentially receiving upstream regulation by unknown ligand-like inputs or metabolic state signals (doering2023nuclearhormonereceptor pages 1-2).
| Category | Key findings | Best supporting sources |
|---|---|---|
| Identity/domains | nhr-49 in Caenorhabditis elegans encodes NHR-49, an HNF4-like nuclear hormone receptor transcription factor functionally compared with mammalian HNF4α and PPARα; it has canonical DNA-binding and ligand-binding domains, and GOF mutations map to the LBD. | (doering2023nuclearhormonereceptor pages 1-2, lee2016gainoffunctionallelesin pages 1-2) |
| Molecular function | Sequence-specific nuclear receptor transcription factor that both activates and represses gene programs controlling fatty-acid metabolism; required for fasting and oxidative-stress transcriptional responses and works with MDT-15. Structural modeling supports likely small-molecule interaction via the LBD, but no definitive endogenous ligand is established. | (doering2023nuclearhormonereceptor pages 1-2, lee2016gainoffunctionallelesin pages 1-2, hu2018thecaenorhabditiselegans pages 1-5) |
| Partners/cofactors | Validated partners include MDT-15 as coactivator, NHR-80 for desaturase gene activation, and NHR-66 for repressive lipid-remodeling and sphingolipid programs; NHR-13 also contributes to desaturase regulation without confirmed direct physical interaction. Yeast two-hybrid using NHR-49-LBD recovered 24 independent cDNAs from 13 genes. | (pathare2012coordinateregulationof pages 2-3, pathare2012coordinateregulationof pages 14-15) |
| Tissue/cellular localization | Broadly expressed in multiple tissues, including intestine and neurons. Cell-specific rescue places key functions in URX/AQR/PQR body-cavity neurons for pathogen avoidance and calcium control, and in intestine for proteostasis and stress programs; hypoxia studies also tested rescue in hypodermis, neurons, and muscle. GOF substitutions did not alter measured subcellular localization. | (lee2016gainoffunctionallelesin pages 1-2, kwon2024regulatoroflipid pages 1-2, sala2024nuclearreceptorsignaling pages 7-8, doering2022nuclearhormonereceptor pages 8-11) |
| Key pathways/targets | Major outputs include mitochondrial and peroxisomal β-oxidation genes acs-2, cpt-5, ech-1; fatty-acid desaturases fat-5, fat-6, fat-7; sphingolipid and lipid-remodeling genes; glyoxylate cycle gene icl-1; lipid transport genes lbp-1, lbp-8; and stress or immune genes including fmo-2 and gst-4. It also supports autophagy-linked hypoxia adaptation and neuronal lipid homeostasis. | (pathare2012coordinateregulationof pages 1-2, lee2016functionalcharacterizationof pages 22-26, pathare2012coordinateregulationof pages 2-3, hu2018thecaenorhabditiselegans pages 1-5, doering2022nuclearhormonereceptor pages 8-11) |
| Phenotypes | Loss of nhr-49 causes high fat, impaired fasting response, shortened lifespan, altered mitochondrial morphology and function, defective pathogen avoidance, and increased sensitivity to oxidative stress, hypoxia, and infection. GOF alleles are functionally distinct and can produce long-, short-, or normal-lifespan outcomes depending on allele. | (pathare2012coordinateregulationof pages 1-2, lee2016gainoffunctionallelesin pages 1-2, hu2018thecaenorhabditiselegans pages 1-5, kwon2024regulatoroflipid pages 1-2) |
| Recent 2023-2024 developments | 2023: review consolidates NHR-49 as a core stress-resilience and healthy-aging regulator; glucose-restriction longevity requires non-cell-autonomous PAQR-2/NHR-49/Δ9-desaturase signaling. 2024: NHR-49 and MDT-15 were shown to couple lipid homeostasis to HSF-1 proteostasis; neuronal NHR-49 in URX/AQR/PQR tunes calcium dynamics and PA14 avoidance; free long-chain fatty acids were proposed to activate NHR-49/80 signaling to initiate development. | (doering2023nuclearhormonereceptor pages 1-2, sala2024nuclearreceptorsignaling pages 1-2, kwon2024regulatoroflipid pages 1-2, sala2024nuclearreceptorsignaling pages 7-8, jeong2023anewampk pages 9-10) |
| Quantitative data points | Microarray cutoff: absolute log2 ratio at least 0.848 and p ≤ 0.001 for NHR-49-regulated genes. Oleic acid rescue: 300 µM OA improved avoidance and URX calcium kinetics. Calcium imaging: trials with max ΔF/F0 < 300% were excluded. Proteostasis: intestinal NHR-49 activation reduced Q35 aggregates by 30% at day 5 adulthood. Hypoxia: after 24 h at 0.5% O2, about 86% WT embryos reached L4; after 48 h, about 44% WT reached L4. Autophagy-pathway perturbations lowered hypoxia survival to 27–44% versus 79% EV control. | (pathare2012coordinateregulationof pages 1-2, kwon2024regulatoroflipid pages 2-4, kwon2024regulatoroflipid pages 9-11, sala2024nuclearreceptorsignaling pages 7-8, doering2022nuclearhormonereceptor pages 8-11, doering2022nuclearhormonereceptor media de728d3f) |
Table: This table summarizes verified identity, molecular function, pathways, localization, phenotypes, and recent 2023-2024 findings for C. elegans NHR-49/UniProt O45666. It provides a concise evidence map for functional annotation with supporting citation IDs.
Cropped figure panels supporting the quantitative hypoxia survival and autophagy-foci conclusions are available from the eLife 2022 paper (doering2022nuclearhormonereceptor media de728d3f, doering2022nuclearhormonereceptor media 16c37f01, doering2022nuclearhormonereceptor media 19a845b3).
References
(doering2023nuclearhormonereceptor pages 1-2): Kelsie R. S. Doering, Glafira Ermakova, and Stefan Taubert. Nuclear hormone receptor nhr-49 is an essential regulator of stress resilience and healthy aging in caenorhabditis elegans. Frontiers in Physiology, Aug 2023. URL: https://doi.org/10.3389/fphys.2023.1241591, doi:10.3389/fphys.2023.1241591. This article has 27 citations.
(pathare2012coordinateregulationof pages 2-3): Pranali P. Pathare, Alex Lin, Karin E. Bornfeldt, Stefan Taubert, and Marc R. Van Gilst. Coordinate regulation of lipid metabolism by novel nuclear receptor partnerships. PLoS Genetics, 8:e1002645, Apr 2012. URL: https://doi.org/10.1371/journal.pgen.1002645, doi:10.1371/journal.pgen.1002645. This article has 139 citations and is from a domain leading peer-reviewed journal.
(pathare2012coordinateregulationof pages 14-15): Pranali P. Pathare, Alex Lin, Karin E. Bornfeldt, Stefan Taubert, and Marc R. Van Gilst. Coordinate regulation of lipid metabolism by novel nuclear receptor partnerships. PLoS Genetics, 8:e1002645, Apr 2012. URL: https://doi.org/10.1371/journal.pgen.1002645, doi:10.1371/journal.pgen.1002645. This article has 139 citations and is from a domain leading peer-reviewed journal.
(hu2018thecaenorhabditiselegans pages 1-5): Queenie Hu, Dayana R D’Amora, Lesley T MacNeil, Albertha J M Walhout, and Terrance J Kubiseski. The caenorhabditis elegans oxidative stress response requires the nhr-49 transcription factor. G3 Genes|Genomes|Genetics, 8:3857-3863, Dec 2018. URL: https://doi.org/10.1534/g3.118.200727, doi:10.1534/g3.118.200727. This article has 51 citations.
(sala2024nuclearreceptorsignaling pages 1-2): Ambre J. Sala, Rogan A. Grant, Ghania Imran, Claire Morton, Renee M. Brielmann, Szymon Gorgoń, Jennifer Watts, Laura C. Bott, and Richard I. Morimoto. Nuclear receptor signaling via nhr-49/mdt-15 regulates stress resilience and proteostasis in response to reproductive and metabolic cues. Genes & Development, May 2024. URL: https://doi.org/10.1101/gad.351829.124, doi:10.1101/gad.351829.124. This article has 9 citations and is from a highest quality peer-reviewed journal.
(lee2016gainoffunctionallelesin pages 1-2): Kayoung Lee, Grace Ying Shyen Goh, Marcus Andrew Wong, Tara Leah Klassen, and Stefan Taubert. Gain-of-function alleles in caenorhabditis elegans nuclear hormone receptor nhr-49 are functionally distinct. PLoS ONE, 11:e0162708, Sep 2016. URL: https://doi.org/10.1371/journal.pone.0162708, doi:10.1371/journal.pone.0162708. This article has 44 citations and is from a peer-reviewed journal.
(kwon2024regulatoroflipid pages 9-11): Saebom Kwon, Kyu-Sang Park, and Kyoung-hye Yoon. Regulator of lipid metabolism nhr-49 mediates pathogen avoidance through precise control of neuronal activity. Cells, 13:978, Jun 2024. URL: https://doi.org/10.3390/cells13110978, doi:10.3390/cells13110978. This article has 3 citations.
(kwon2024regulatoroflipid pages 1-2): Saebom Kwon, Kyu-Sang Park, and Kyoung-hye Yoon. Regulator of lipid metabolism nhr-49 mediates pathogen avoidance through precise control of neuronal activity. Cells, 13:978, Jun 2024. URL: https://doi.org/10.3390/cells13110978, doi:10.3390/cells13110978. This article has 3 citations.
(sala2024nuclearreceptorsignaling pages 7-8): Ambre J. Sala, Rogan A. Grant, Ghania Imran, Claire Morton, Renee M. Brielmann, Szymon Gorgoń, Jennifer Watts, Laura C. Bott, and Richard I. Morimoto. Nuclear receptor signaling via nhr-49/mdt-15 regulates stress resilience and proteostasis in response to reproductive and metabolic cues. Genes & Development, May 2024. URL: https://doi.org/10.1101/gad.351829.124, doi:10.1101/gad.351829.124. This article has 9 citations and is from a highest quality peer-reviewed journal.
(doering2022nuclearhormonereceptor pages 8-11): Kelsie RS Doering, Xuanjin Cheng, Luke Milburn, Ramesh Ratnappan, Arjumand Ghazi, Dana L Miller, and Stefan Taubert. Nuclear hormone receptor nhr-49 acts in parallel with hif-1 to promote hypoxia adaptation in caenorhabditis elegans. eLife, Mar 2022. URL: https://doi.org/10.7554/elife.67911, doi:10.7554/elife.67911. This article has 29 citations and is from a domain leading peer-reviewed journal.
(pathare2012coordinateregulationof pages 1-2): Pranali P. Pathare, Alex Lin, Karin E. Bornfeldt, Stefan Taubert, and Marc R. Van Gilst. Coordinate regulation of lipid metabolism by novel nuclear receptor partnerships. PLoS Genetics, 8:e1002645, Apr 2012. URL: https://doi.org/10.1371/journal.pgen.1002645, doi:10.1371/journal.pgen.1002645. This article has 139 citations and is from a domain leading peer-reviewed journal.
(jeong2023anewampk pages 9-10): Jin-Hyuck Jeong, Jun-Seok Han, Youngae Jung, Seung-Min Lee, So-Hyun Park, Mooncheol Park, Min-Gi Shin, Nami Kim, Mi Sun Kang, Seokho Kim, Kwang-Pyo Lee, Ki-Sun Kwon, Chun-A. Kim, Yong Ryoul Yang, Geum-Sook Hwang, and Eun-Soo Kwon. A new ampk isoform mediates glucose-restriction induced longevity non-cell autonomously by promoting membrane fluidity. Nature Communications, Jan 2023. URL: https://doi.org/10.1038/s41467-023-35952-z, doi:10.1038/s41467-023-35952-z. This article has 41 citations and is from a highest quality peer-reviewed journal.
(kwon2024regulatoroflipid pages 2-4): Saebom Kwon, Kyu-Sang Park, and Kyoung-hye Yoon. Regulator of lipid metabolism nhr-49 mediates pathogen avoidance through precise control of neuronal activity. Cells, 13:978, Jun 2024. URL: https://doi.org/10.3390/cells13110978, doi:10.3390/cells13110978. This article has 3 citations.
(doering2022nuclearhormonereceptor media de728d3f): Kelsie RS Doering, Xuanjin Cheng, Luke Milburn, Ramesh Ratnappan, Arjumand Ghazi, Dana L Miller, and Stefan Taubert. Nuclear hormone receptor nhr-49 acts in parallel with hif-1 to promote hypoxia adaptation in caenorhabditis elegans. eLife, Mar 2022. URL: https://doi.org/10.7554/elife.67911, doi:10.7554/elife.67911. This article has 29 citations and is from a domain leading peer-reviewed journal.
(lee2016functionalcharacterizationof pages 22-26): Ka Young Lee. Functional characterization of gene regulation by nhr-49. ArXiv, Jan 2016. URL: https://doi.org/10.14288/1.0305709, doi:10.14288/1.0305709. This article has 0 citations.
(doering2022nuclearhormonereceptor media 16c37f01): Kelsie RS Doering, Xuanjin Cheng, Luke Milburn, Ramesh Ratnappan, Arjumand Ghazi, Dana L Miller, and Stefan Taubert. Nuclear hormone receptor nhr-49 acts in parallel with hif-1 to promote hypoxia adaptation in caenorhabditis elegans. eLife, Mar 2022. URL: https://doi.org/10.7554/elife.67911, doi:10.7554/elife.67911. This article has 29 citations and is from a domain leading peer-reviewed journal.
(doering2022nuclearhormonereceptor media 19a845b3): Kelsie RS Doering, Xuanjin Cheng, Luke Milburn, Ramesh Ratnappan, Arjumand Ghazi, Dana L Miller, and Stefan Taubert. Nuclear hormone receptor nhr-49 acts in parallel with hif-1 to promote hypoxia adaptation in caenorhabditis elegans. eLife, Mar 2022. URL: https://doi.org/10.7554/elife.67911, doi:10.7554/elife.67911. This article has 29 citations and is from a domain leading peer-reviewed journal.