ArticlePhysiological reports2015
Generation of Kcnma1fl-tdTomato, a conditional deletion of the BK channel α subunit in mouse.
Article in Physiological reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 14 citations in OpenAlex.
- The genetics of smoking in individuals with chronic obstructive pulmonary disease.Respiratory research · 2018Trial
- Renal NHE3 is required to limit hypokalemia and metabolic acidosis during dietary potassium deficiency.Pflugers Archiv : European journal of physiology · 2026Article
- Vasoprotective Effects of Hyperoside against Cerebral Ischemia/Reperfusion Injury in Rats: Activation of Large-Conductance CaNeural plasticity · 2023Article
- Emodepside targets SLO-1 channels of Onchocerca ochengi and induces broad anthelmintic effects in a bovine model of onchocerciasis.PLoS pathogens · 2021Article
- Effects of Single Nucleotide Polymorphisms in HumanFrontiers in molecular neuroscience · 2019Article
- Glutamate-activated BK channel complexes formed with NMDA receptors.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Distinct Effects of CaInternational journal of biological sciences · 2017Article
- Cartilage-Specific Knockout of the Mechanosensory Ion Channel TRPV4 Decreases Age-Related Osteoarthritis.Scientific reports · 2016Article
- Generation of a Wt1 conditional deletion, nuclear red fluorescent protein reporter allele in the mouse.Differentiation; research in biological diversityArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
BK large conductance calcium-activated K(+) channels (KC a1.1) are expressed widely across many tissues, contributing to systemic regulation of cardiovascular, neurological, and other specialized physiological functions. The pore-forming α subunit is encoded by the Kcnma1 gene, originally named mSlo1 in mouse and slowpoke in Drosophila. Global deletion in mouse (Kcnma1(-/-)) produces a plethora of defects in neuron and muscle excitability, as well as other phenotypes related to channel function in nonexcitable cells. While homozygous null mice are viable, the ubiquitous loss of BK function has complicated the interpretation of phenotypes involving the interaction of multiple cell types which independently express BK channels. Here, we report the generation of a targeted allele for conditional inactivation of Kcnma1 using the Cre-loxP system (Kcnma1(fl)-tdTomato). Cre-mediated recombination generates a null allele, and BK currents were not detectable in neurons and muscle cells from Nestin-Cre; Kcnma1(fl/fl) and SM22α-Cre; Kcnma1(fl/fl) mice, respectively. tdTomato expression was detected in Cre-expressing tissues, but not in Cre-negative controls. These data demonstrate the utility of Kcnma1(fl)-tdTomato for conditional deletion of the BK channel, facilitating the understanding of tissue-specific contributions to physiological function in vivo.
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.