ArticleProceedings of the National Academy of Sciences of the United States of America2011
Atypical protein kinase C (aPKCzeta and aPKClambda) is dispensable for mammalian hematopoietic stem cell activity and blood formation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 36 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
36 citing papers in PubMed, 48 citations in OpenAlex.
- Review
- PKC isoforms in hematopoietic lineages and myeloid/lymphoid leukemias: mechanistic insights and therapeutic prospects.Frontiers in oncology · 2026Review
- Cell polarity: cell type-specific regulators, common pathways, and polarized vesicle transport.Leukemia · 2025Review
- Article
- Hes1 deficiency causes hematopoietic stem cell exhaustion.Stem cells (Dayton, Ohio) · 2020Article
- The Dual Roles of the Atypical Protein Kinase Cs in Cancer.Cancer cell · 2019Review
- The signaling axis atypical protein kinase C λ/ι-Satb2 mediates leukemic transformation of B-cell progenitors.Nature communications · 2019Article
- Attenuation of PKCδ enhances metabolic activity and promotes expansion of blood progenitors.The EMBO journal · 2018Article
- Diverging impact of cell fate determinants Scrib and Llgl1 on adhesion and migration of hematopoietic stem cells.Journal of cancer research and clinical oncology · 2018Article
- Signaling Pathways Regulating Hematopoietic Stem Cell and Progenitor Aging.Current stem cell reports · 2018Article
- The cell fate determinant Scribble is required for maintenance of hematopoietic stem cell function.Leukemia · 2018Article
- Lymphocyte Fate and Metabolism: A Clonal Balancing Act.Trends in cell biology · 2017Review
- Article
- p190-B RhoGAP and intracellular cytokine signals balance hematopoietic stem and progenitor cell self-renewal and differentiation.Nature communications · 2017Article
- Lethal giant larvae-1 deficiency enhances the CD8(+) effector T-cell response to antigen challenge in vivo.Immunology and cell biology · 2016Article
- Adhesion receptors involved in HSC and early-B cell interactions with bone marrow microenvironment.Cellular and molecular life sciences : CMLS · 2016Review
- Asymmetric PI3K Signaling Driving Developmental and Regenerative Cell Fate Bifurcation.Cell reports · 2015Article
- Atypical PKC-iota Controls Stem Cell Expansion via Regulation of the Notch Pathway.Stem cell reports · 2015Article
- Asymmetric Cell Division in T Lymphocyte Fate Diversification.Trends in immunology · 2015Review
- p62 is required for stem cell/progenitor retention through inhibition of IKK/NF-κB/Ccl4 signaling at the bone marrow macrophage-osteoblast niche.Cell reports · 2014Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
Abstract
The stem-cell pool is considered to be maintained by a balance between symmetric and asymmetric division of stem cells. The cell polarity model proposes that the facultative use of symmetric and asymmetric cell division is orchestrated by a polarity complex consisting of partitioning-defective proteins Par3 and Par6, and atypical protein kinase C (aPKCζ and aPKCλ), which regulates planar symmetry of dividing stem cells with respect to the signaling microenvironment. However, the role of the polarity complex is unexplored in mammalian adult stem-cell functions. Here we report that, in contrast to accepted paradigms, polarization and activity of adult hematopoietic stem cell (HSC) do not depend on either aPKCζ or aPKCλ or both in vivo. Mice, having constitutive and hematopoietic-specific (Vav1-Cre) deletion of aPKCζ and aPKCλ, respectively, have normal hematopoiesis, including normal HSC self-renewal, engraftment, differentiation, and interaction with the bone marrow microenvironment. Furthermore, inducible complete deletion of aPKCλ (Mx1-Cre) in aPKCζ(-/-) HSC does not affect HSC polarization, self-renewal, engraftment, or lineage repopulation. In addition, aPKCζ- and aPKCλ-deficient HSCs elicited a normal pattern of hematopoietic recovery secondary to myeloablative stress. Taken together, the expression of aPKCζ, aPKCλ, or both are dispensable for primitive and adult HSC fate determination in steady-state and stress hematopoiesis, contrary to the hypothesis of a unique, evolutionary conserved aPKCζ/λ-directed cell polarity signaling mechanism in mammalian HSC fate determination.
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.