ArticleThe Journal of experimental medicine2016
Senp1 drives hypoxia-induced polycythemia via GATA1 and Bcl-xL in subjects with Monge's disease.
Article in The Journal of experimental medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 39 citations in OpenAlex.
- Genome-wide association study of somatic GATA1s mutations in newborns with Down syndrome.Blood advances · 2025Article
- Advances in Understanding Adaptive Hemoglobin Concentration at High Altitude.American journal of human biology : the official journal of the Human Biology Council · 2025Article
- Life destiny of erythrocyte in high altitude erythrocytosis: mechanisms underlying the progression from physiological (moderate) to pathological (excessive) high-altitude erythrocytosis.Frontiers in genetics · 2025Review
- Plasma-based transcriptomic non-coding signature for predicting relapse in pediatric acute lymphoblastic leukemia.Heliyon · 2024Article
- Altitude illnesses.Nature reviews. Disease primers · 2024Review
- High altitude polycythemia and its maladaptive mechanisms: an updated review.Frontiers in medicine · 2024Review
- Long noncoding RNA HIKER regulates erythropoiesis in Monge's disease via CSNK2B.The Journal of clinical investigation · 2023Article
- Preserved peak exercise capacity in Andean highlanders with excessive erythrocytosis both before and after isovolumic hemodilution.Journal of applied physiology (Bethesda, Md. : 1985) · 2023Article
- High-Altitude Erythrocytosis: Mechanisms of Adaptive and Maladaptive Responses.Physiology (Bethesda, Md.) · 2022Review
- ARID1B, a molecular suppressor of erythropoiesis, is essential for the prevention of Monge's disease.Experimental & molecular medicine · 2022Article
- Physiological Genomics of Adaptation to High-Altitude Hypoxia.Annual review of animal biosciences · 2021Review
- Multiple mechanisms drive genomic adaptation to extreme ONature communications · 2021Article
- The genome-wide impact of trisomy 21 on DNA methylation and its implications for hematopoiesis.Nature communications · 2021Article
- Protective role of estrogen against excessive erythrocytosis in Monge's disease.Experimental & molecular medicine · 2021Article
- Mechanistic and Translational Advances Using iPSC-Derived Blood Cells.Journal of Experimental Pathology · 2020Article
- Increased hypoxic proliferative response and gene expression in erythroid progenitor cells of Andean highlanders with chronic mountain sickness.American journal of physiology. Regulatory, integrative and comparative physiology · 2020Article
- Neuroprotective Role of Akt in Hypoxia Adaptation in Andeans.Frontiers in neuroscience · 2020Article
- The Immune Landscape of Thyroid Cancer in the Context of Immune Checkpoint Inhibition.International journal of molecular sciences · 2019Review
- Novel insight into the genetic basis of high-altitude pulmonary hypertension in Kyrgyz highlanders.European journal of human genetics : EJHG · 2019Article
- Mitochondrial dysfunction in iPSC-derived neurons of subjects with chronic mountain sickness.Journal of applied physiology (Bethesda, Md. : 1985) · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
In this study, because excessive polycythemia is a predominant trait in some high-altitude dwellers (chronic mountain sickness [CMS] or Monge's disease) but not others living at the same altitude in the Andes, we took advantage of this human experiment of nature and used a combination of induced pluripotent stem cell technology, genomics, and molecular biology in this unique population to understand the molecular basis for hypoxia-induced excessive polycythemia. As compared with sea-level controls and non-CMS subjects who responded to hypoxia by increasing their RBCs modestly or not at all, respectively, CMS cells increased theirs remarkably (up to 60-fold). Although there was a switch from fetal to adult HgbA0 in all populations and a concomitant shift in oxygen binding, we found that CMS cells matured faster and had a higher efficiency and proliferative potential than non-CMS cells. We also established that SENP1 plays a critical role in the differential erythropoietic response of CMS and non-CMS subjects: we can convert the CMS phenotype into that of non-CMS and vice versa by altering SENP1 levels. We also demonstrated that GATA1 is an essential downstream target of SENP1 and that the differential expression and response of GATA1 and Bcl-xL are a key mechanism underlying CMS pathology.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.