ReviewCell death and differentiation2009
Of the atypical PKCs, Par-4 and p62: recent understandings of the biology and pathology of a PB1-dominated complex.
Review in Cell death and differentiation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 81 citations in OpenAlex.
- Protein kinase C iota (PKCι) and pVHL are both needed for lysosomal degradation of α5 integrin in renal carcinoma cells.Molecular biology reports · 2025Article
- Possible prognostic impact of PKCι genetic variants in prostate cancer.Cancer cell international · 2024Article
- PKCι induces differential phosphorylation of STAT3 to modify STAT3-related signaling pathways in pancreatic cancer cells.Journal of cell communication and signaling · 2023Article
- Kinase regulation by liquid-liquid phase separation.Trends in cell biology · 2023Review
- A novel non‑selective atypical PKC agonist could protect neuronal cell line from Aβ‑oligomer induced toxicity by suppressing Aβ generation.Molecular medicine reports · 2022Article
- Atypical protein kinase C is essential for embryonic vascular development in mice.Genesis (New York, N.Y. : 2000) · 2021Article
- Plasticity of Paneth cells and their ability to regulate intestinal stem cells.Stem cell research & therapy · 2020Review
- The Dual Roles of the Atypical Protein Kinase Cs in Cancer.Cancer cell · 2019Review
- TAK1 converts Sequestosome 1/p62 from an autophagy receptor to a signaling platform.EMBO reports · 2019Article
- The signaling axis atypical protein kinase C λ/ι-Satb2 mediates leukemic transformation of B-cell progenitors.Nature communications · 2019Article
- PEX5 regulates autophagy via the mTORC1-TFEB axis during starvation.Experimental & molecular medicine · 2018Article
- aPKC: the Kinase that Phosphorylates Cell Polarity.F1000Research · 2018Review
- PKCζ as a promising therapeutic target for TNFα-induced inflammatory disorders in chronic cutaneous wounds.International journal of molecular medicine · 2017Article
- Downregulation of PKCζ/Pard3/Pard6b is responsible for lung adenocarcinoma cell EMT and invasion.Cellular signalling · 2017Article
- PKCζ phosphorylates TRAF2 to protect against intestinal ischemia-reperfusion-induced injury.Cell death & disease · 2017Article
- Flow signaling and atherosclerosis.Cellular and molecular life sciences : CMLS · 2017Review
- Autophagy controls centrosome number by degrading Cep63.Nature communications · 2016Article
- Control of Paneth Cell Fate, Intestinal Inflammation, and Tumorigenesis by PKCλ/ι.Cell reports · 2016Article
- The Mammalian Blood-Testis Barrier: Its Biology and Regulation.Endocrine reviews · 2015Review
- PKCζ Promotes Breast Cancer Invasion by Regulating Expression of E-cadherin and Zonula Occludens-1 (ZO-1) via NFκB-p65.Scientific reports · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The recent identification of a novel protein-protein interaction module, termed PB1, in critical signaling molecules such as p62 (also known as sequestosome1), the atypical PKCs, and Par-6, has unveiled the existence of a new set of signaling complexes, which can be central to several biological processes from development to cancer. In this review, we will discuss the most recent advances on the role that the different components of these complexes have in vivo and that are relevant to human disease. In particular, we will review what we are learning from new data from knockout mice, and the indications from human mutations on the real role of these proteins in the physiology and biology of human diseases. The role that PKCzeta, PKClambda/iota, and Par-4 have in lung and prostate cancer in vivo and in humans will be extensively covered in this article, as will the multifunctional role of p62 as a novel hub in cell signaling during cancer and inflammation, and the mechanistic details and controversial data published on its potential role in aggregate formation and signaling. All this published information is shedding new light on the proposed pathological implications of these PB1-regulators in disease and shows their important role in cell physiology.
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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.