ArticleThe Journal of cell biology1995
Transforming growth factor-alpha and beta-amyloid precursor protein share a secretory mechanism.
Article in The Journal of cell biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 160 citations in OpenAlex.
- Glycosaminoglycan modifications of betaglycan regulate ectodomain shedding to fine-tune TGF-β signaling responses in ovarian cancer.Cell communication and signaling : CCS · 2024Article
- Secretome and Tunneling Nanotubes: A Multilevel Network for Long Range Intercellular Communication between Endothelial Cells and Distant Cells.International journal of molecular sciences · 2021Review
- Dynamics of Axl Receptor Shedding in Hepatocellular Carcinoma and Its Implication for Theranostics.International journal of molecular sciences · 2018Review
- Characterization of the catalytic properties of the membrane-anchored metalloproteinase ADAM9 in cell-based assays.The Biochemical journal · 2017Article
- SheddomeDB: the ectodomain shedding database for membrane-bound shed markers.BMC bioinformatics · 2017Review
- Functional Differences of Very-Low-Density Lipoprotein Receptor Splice Variants in Regulating Wnt Signaling.Molecular and cellular biology · 2016Article
- Role of ADAM17 in the non-cell autonomous effects of oncogene-induced senescence.Breast cancer research : BCR · 2015Article
- Inside-out Regulation of Ectodomain Cleavage of Cluster-of-Differentiation-44 (CD44) and of Neuregulin-1 Requires Substrate Dimerization.The Journal of biological chemistry · 2015Article
- The sorting protein PACS-2 promotes ErbB signalling by regulating recycling of the metalloproteinase ADAM17.Nature communications · 2015Article
- Microfabricated collagen tracks facilitate single cell metastatic invasion in 3D.Integrative biology : quantitative biosciences from nano to macro · 2013Article
- Dominant-negative effect of truncated mannose 6-phosphate/insulin-like growth factor II receptor species in cancer.The FEBS journal · 2012Article
- Interleukin-1 stimulates ADAM17 through a mechanism independent of its cytoplasmic domain or phosphorylation at threonine 735.PloS one · 2012Article
- Shedding of syndecan-1 from human hepatocytes alters very low density lipoprotein clearance.Hepatology (Baltimore, Md.) · 2012Article
- Release of membrane-associated L-dopa decarboxylase from human cells.Neurochemical research · 2011Article
- ADAM17 is regulated by a rapid and reversible mechanism that controls access to its catalytic site.Journal of cell science · 2010Article
- Roles for the type III TGF-beta receptor in human cancer.Cellular signalling · 2010Review
- Molecular and cellular mechanisms of ectodomain shedding.Anatomical record (Hoboken, N.J. : 2007) · 2010Review
- Mitochondrial reactive oxygen species mediate GPCR-induced TACE/ADAM17-dependent transforming growth factor-alpha shedding.Molecular biology of the cell · 2009Article
- Neurotrophins induce neuregulin release through protein kinase Cdelta activation.The Journal of biological chemistry · 2009Article
- The role of protease activity in ErbB biology.Experimental cell research · 2009Review
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
Cleavage and release of membrane protein ectodomains, a regulated process that affects many cell surface proteins, remains largely uncharacterized. To investigate whether cell surface proteins are cleaved through a shared mechanism or through multiple independent mechanisms, we mutagenized Chinese hamster ovary (CHO) cells and selected clones that were unable to cleave membrane-anchored transforming growth factor alpha (TGF-alpha). The defect in TGF-alpha cleavage in these clones is most apparent upon cell treatment with the protein kinase C (PKC) activator PMA, which stimulates TGF-alpha cleavage in wild-type cells. The mutant clones do not have defects in TFG-alpha expression, transport to the cell surface or turnover. Concomitant with the loss of TGF-alpha cleavage, these clones have lost the ability to cleave many structurally unrelated membrane proteins in response to PMA. These proteins include beta-amyloid precursor protein (beta-APP), whose cleavage into a secreted form avoids conversion into the amyloidogenic peptide A beta, and a group of cell surface proteins whose release into the medium is stimulated by PMA in wild type CHO cells but not in mutants. The mutations prevent cleavage by PKC-dependent as well as PKC-independent mechanisms, and thus affect an essential component that functions downstream of these various signaling mechanisms. We propose that regulated cleavage and secretion of membrane protein ectodomains is mediated by a common system whose components respond to multiple activators and act on susceptible proteins of diverse structure and function.
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.