ArticleThe Journal of steroid biochemistry and molecular biology2010
Expression of MAP3 kinase COT1 is up-regulated by 1,25-dihydroxyvitamin D3 in parallel with activated c-jun during differentiation of human myeloid leukemia cells.
Article in The Journal of steroid biochemistry and molecular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 8 citations in OpenAlex.
- Cell-Type-Specific Effects of Silibinin on Vitamin D-Induced Differentiation of Acute Myeloid Leukemia Cells Are Associated with Differential Modulation of RXRα Levels.Leukemia research and treatment · 2012Article
- Oncoprotein Cot1 represses kinase suppressors of Ras1/2 and 1,25-dihydroxyvitamin D3-induced differentiation of human acute myeloid leukemia cells.Journal of cellular physiology · 2011Article
- RB in breast cancer: differential effects in estrogen receptor-positive and estrogen receptor-negative disease.Cell cycle (Georgetown, Tex.) · 2010Article
- Inhibition of Cot1/Tlp2 oncogene in AML cells reduces ERK5 activation and up-regulates p27Kip1 concomitant with enhancement of differentiation and cell cycle arrest induced by silibinin and 1,25-dihydroxyvitamin D(3).Cell cycle (Georgetown, Tex.) · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The role of MAP kinase pathways in 1,25-dihydroxyvitamin D3 (1,25D)-induced differentiation of myeloid leukemia cells is well established, but the mechanisms by which 1,25D activates these pathways are not entirely clear. Following the finding that kinase suppressors of ras (KSR) 1 and 2 are directly regulated by 1,25D and participate in the monocytic differentiation process, we investigated if the COT1 oncogene (Tpl2 in the rat), known to interact with human KSR2 (hKSR2), is also involved in 1,25D-induced differentiation in leukemia cells. Here we report that the exposure of HL60 and U937 myeloid leukemia cells to 1,25D increases COT1 expression in a concentration-dependent manner. However, COT1 appears to have a differentiation-limiting role in these cells, as an exposure of HL60 and U937 cells to a pharmacological inhibitor of COT1 kinase activity, 4-(3-chloro-4-fluorophenylamino)-6-(pyridin-3-yl-methylamino-3-cyano-[1-7]-naphthyridine, results in increased 1,25D-induced differentiation. These findings provide an additional insight into the 1,25D-regulation of MAPK pathways that contribute to monocytic differentiation process of myeloid leukemia cells.
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.