ReviewSeminars in immunopathology2012
Myeloproliferation and hematopoietic stem cell dysfunction due to defective Notch receptor modification by O-fucose glycans.
Review in Seminars in immunopathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 3 citations in OpenAlex.
- Essential cell-intrinsic requirement for GMDS in T cell development.Frontiers in immunology · 2025Article
- NOTCH-1 Gene Mutations Influence Survival in Acute Myeloid Leukemia Patients.Asian Pacific journal of cancer prevention : APJCP · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
O-fucosylglycans on Notch extracellular domain epidermal growth factor (EGF) repeats are critical in modulating Notch signaling by altering the sensitivity of Notch receptors to activation by Notch ligands. Mice lacking Notch O-fucosylglycans display granulo-monocytic myeloproliferation, hematopoietic stem cell dysfunction and aberrant stem cell niche occupancy. The inability of the stem cells/progenitors that lack Notch O-fucosylglycans to transcribe Notch signaling activation is attributed by a loss of effective Notch-ligand interaction. These findings, in conjunction with myeloproliferation identified in mouse models with defective Notch cleavage or ligand endocytosis, reveal emerging new roles of Notch in hematopoietic stem cell biology and myeloid homeostasis.
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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.