ArticleExperimental & molecular medicine2018
A splice variant of human Bmal1 acts as a negative regulator of the molecular circadian clock.
Article in Experimental & molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 201 citations in OpenAlex.
- Genome-wide association study of more than 40,000 bipolar disorder cases provides new insights into the underlying biology.Nature genetics · 2021Pooled it
- BMAL1 in cardiovascular diseases: Molecular mechanisms, circadian regulation and translational perspectives (Review).Molecular medicine reports · 2026Review
- PANoptosis as a drug discovery framework: integrating cell death architecture with clinical translation.Genes and immunity · 2026Review
- Targeting PANoptosis in atherosclerosis: bridging cell death mechanisms and therapy.Apoptosis : an international journal on programmed cell death · 2026Review
- Core Circadian Protein BMAL1: Implication for Nervous System Functioning and Its Diseases.Brain sciences · 2025Review
- Structurally and functionally optimized silk fibroin-alginate-based biomimetic scaffolds reinforced with nanobioceramics for bone tissue engineering applications.Journal of nanobiotechnology · 2025Article
- Targeting PANoptosis: a promising therapeutic strategy for ALI/ARDS.Apoptosis : an international journal on programmed cell death · 2025Review
- Emerging new immune checkpoint inhibitors in solid tumor immunotherapy.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Fine mapping and prediction of a candidate gene for wrinkled rind in melon (Cucumis melo L.).TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2025Article
- Ocean acidification induces changes in circadian alternative splicing profiles in a coral reef fish.Scientific reports · 2025Article
- Emerging Roles of Eosinophils in Bone.Current osteoporosis reports · 2025Review
- Crosstalk Between Cell Death and Spinal Cord Injury: Neurology and Therapy.Molecular neurobiology · 2024Review
- The role of circular RNA targeting IGF2BPs in cancer-a potential target for cancer therapy.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Prediction value of pericoronary fat attenuation index for coronary in-stent restenosis.European radiology · 2024Article
- Ubiquitination and deubiquitination in the regulation of NJournal of molecular medicine (Berlin, Germany) · 2024Review
- Necroptosis inhibitors: mechanisms of action and therapeutic potential.Apoptosis : an international journal on programmed cell death · 2024Review
- TRIM25 inhibition attenuates inflammation, senescence, and oxidative stress in microvascular endothelial cells induced by hyperglycemia.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2024Article
- 24S-Hydroxycholesterol in Neuropsychiatric Diseases: Schizophrenia, Autism Spectrum Disorder, and Bipolar Disorder.Advances in experimental medicine and biology · 2024Article
- Distinct and targetable role of calcium-sensing receptor in leukaemia.Nature communications · 2023Article
- A novel murine model of mania.Molecular psychiatry · 2023Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bmal1 is one of the key molecules that controls the mammalian molecular clock. In humans, two isoforms of Bmal1 are generated by alternative RNA splicing. Unlike the extensively studied hBmal1b, the canonical form of Bmal1 in most species, the expression and/or function of another human-specific isoform, hBmal1a, are poorly understood. Due to the lack of the N-terminal nuclear localization signal (NLS), hBMAL1a does not enter the nucleus as hBMAL1b does. However, despite the lack of the NLS, hBMAL1a still dimerizes with either hCLOCK or hBMAL1b and thereby promotes cytoplasmic retention or protein degradation, respectively. Consequently, hBMAL1a interferes with hCLOCK:hBMAL1b-induced transcriptional activation and the circadian oscillation of Period2. Moreover, when the expression of endogenous hBmal1a is aborted by CRISPR/Cas9-mediated knockout, the rhythmic expression of hPer2 and hBmal1b is restored in cultured HeLa cells. Together, these results suggest a role for hBMAL1a as a negative regulator of the mammalian molecular clock.
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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.