ArticleJournal of neurochemistry2006
Tissue inhibitor of metalloproteinase-2 (TIMP-2) expression is regulated by multiple neural differentiation signals.
Article in Journal of neurochemistry, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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
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Who cites it
22 citing papers in PubMed, 43 citations in OpenAlex.
- Extracellular Matrix (ECM)-Regulated Molecular Switches: Tissue Inhibitors of Metalloproteinases in Synaptic Formation and Neuropathic Diseases.Cellular and molecular neurobiology · 2025Review
- Serum cytokine profiles at near term-equivalent age and their association with neurodevelopmental outcomes in preterm infants: an exploratory study.Frontiers in pediatrics · 2025Article
- Neuronal TIMP2 regulates hippocampus-dependent plasticity and extracellular matrix complexity.Molecular psychiatry · 2023Article
- Article
- Review
- The role of microglial/macrophagic salt-inducible kinase 3 on normal and excessive phagocytosis after transient focal cerebral ischemia.Cellular and molecular life sciences : CMLS · 2022Article
- Unravelling the distinct biological functions and potential therapeutic applications of TIMP2 in cancer.Carcinogenesis · 2022Review
- Synchronous neuronal interactions in rat hypothalamic culture: a novel model for the study of network dynamics in metabolic disorders.Experimental brain research · 2021Article
- The Roles of Matrix Metalloproteinases and Their Inhibitors in Human Diseases.International journal of molecular sciences · 2020Review
- Deciphering the neuroprotective and neurogenic potential of soluble amyloid precursor protein alpha (sAPPα).Cellular and molecular life sciences : CMLS · 2020Review
- HSV-1 interaction to 3-O-sulfated heparan sulfate in mouse-derived DRG explant and profiles of inflammatory markers during virus infection.Journal of neurovirology · 2017Article
- Acetate supplementation as a means of inducing glioblastoma stem-like cell growth arrest.Journal of cellular physiology · 2015Article
- Triacetin-based acetate supplementation as a chemotherapeutic adjuvant therapy in glioma.International journal of cancer · 2014Article
- Cytokine functions of TIMP-1.Cellular and molecular life sciences : CMLS · 2014Review
- N-acetylaspartate (NAA) and N-acetylaspartylglutamate (NAAG) promote growth and inhibit differentiation of glioma stem-like cells.The Journal of biological chemistry · 2013Article
- Acetate supplementation induces growth arrest of NG2/PDGFRα-positive oligodendroglioma-derived tumor-initiating cells.PloS one · 2013Article
- An integrin-binding N-terminal peptide region of TIMP-2 retains potent angio-inhibitory and anti-tumorigenic activity in vivo.Peptides · 2011Article
- A dual role for microglia in promoting tissue inhibitor of metalloproteinase (TIMP) expression in glial cells in response to neuroinflammatory stimuli.Journal of neuroinflammation · 2011Article
- The tissue inhibitors of metalloproteinases (TIMPs): an ancient family with structural and functional diversity.Biochimica et biophysica acta · 2010Review
- Tissue inhibitors of metalloproteinases in cell signaling: metalloproteinase-independent biological activities.Science signaling · 2008Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Neuronal differentiation requires exquisitely timed cell cycle arrest for progenitors to acquire an appropriate neuronal cell fate and is achieved by communication between soluble signals, such as growth factors and extracellular matrix molecules. Here we report that the expression of TIMP-2, a matrix metalloproteinase inhibitor, is up-regulated by signals that control proliferation (bFGF and EGF) and differentiation (retinoic acid and NGF) in neural progenitor and neuroblastoma cell lines. TIMP-2 expression coincides with the appearance of neurofilament-positive neurons, indicating that TIMP-2 may play a role in neurogenesis. The up-regulation of TIMP-2 expression by proliferate signals suggests a role in the transition from proliferation to neuronal differentiation. Live labeling experiments demonstrate TIMP-2 expression only on alpha(3) integrin-positive cells. Thus, TIMP-2 function may be mediated via interaction with integrin receptor(s). We propose that TIMP-2 represents a component of the neurogenic signaling cascade induced by mitogenic stimuli that may withdraw progenitor cells from the cell cycle permitting their terminal neuronal differentiation.
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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.