ArticleBioarchitecture2012
Parvin-ILK: An intimate relationship.
Article in Bioarchitecture, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
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.
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Who cites it
5 citing papers in PubMed, 22 citations in OpenAlex.
- Parvin is essential for indirect flight muscle (IFM) performance and Zasp52 localisation to the Z-disc in Drosophila melanogaster.Cell and tissue research · 2025Article
- Article
- Neutrophil extracellular traps promote proliferation of pulmonary smooth muscle cells mediated by CCDC25 in pulmonary arterial hypertension.Respiratory research · 2024Article
- Thy-1 (CD90)-regulated cell adhesion and migration of mesenchymal cells: insights into adhesomes, mechanical forces, and signaling pathways.Frontiers in cell and developmental biology · 2023Review
- Drosophila importin-7 functions upstream of the Elmo signaling module to mediate the formation and stability of muscle attachments.Journal of cell science · 2013Article
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
No grant is acknowledged in the PubMed record.
Abstract
Integrin-linked kinase (ILK), PINCH and Parvin proteins form the IPP-complex that has been established as a core component of the integrin-actin link. Our recent genetic studies on Drosophila parvin, reveal that loss of function mutant defects phenocopy those observed upon loss of ILK or PINCH in the muscle and the wing, strengthening the notion that these proteins function together in the organism. Our work identified that ILK is necessary and sufficient for parvin subcellular localization, corroborating previous data indicating a direct association between these two proteins. Further genetic epistasis analysis of the IPP-complex assembly at integrin adhesion sites reveals that depending on the cell context each component is required differently. At the muscle attachment sites of the embryo, ILK is placed upstream in the hierarchy of genetic interactions required for the IPP-complex assembly. By contrast, in the wing epithelium the three proteins are mutually interdependent. Finally, we uncovered a novel property for the CH1-domain of parvin: its recruitment at the integrin-containing junctions in an ILK-dependent manner. Apparently, this ability of the CH1-domain is controlled by the inter-CH linker region. Thus, an intramolecular interaction within parvin could serve as a putative regulatory mechanism controlling the ILK-Parvin interaction.
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.