ArticleScientific reports2017
Redundant functions of I-BAR family members, IRSp53 and IRTKS, are essential for embryonic development.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 27 citations in OpenAlex.
- Breaking cellular boundaries: molecular mechanisms of tunneling nanotube formation and fusion.Biochemical Society transactions · 2026Review
- WAVE complex forms linear arrays at negative membrane curvature to instruct lamellipodia formation.The Journal of cell biology · 2025Article
- CpG methylation changes associated with hyperglycemia in type 1 diabetes occur at angiogenic glomerular and retinal gene loci.Scientific reports · 2025Article
- Insulin receptor tyrosine kinase substrate in health and disease (Review).Molecular medicine reports · 2025Review
- Aging and obesity prime the methylome and transcriptome of adipose stem cells for disease and dysfunction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Hippocampal BAIAP2 prevents chronic mild stress-induced depression-like behaviors in mice.Frontiers in psychiatry · 2023Article
- The WAVE complex associates with sites of saddle membrane curvature.The Journal of cell biology · 2021Article
- Full assembly of HIV-1 particles requires assistance of the membrane curvature factor IRSp53.eLife · 2021Article
- Loss of Baiap2l2 destabilizes the transducing stereocilia of cochlear hair cells and leads to deafness.The Journal of physiology · 2021Article
- IRSp53 controls plasma membrane shape and polarized transport at the nascent lumen in epithelial tubules.Nature communications · 2020Article
- Differential interactions of missing in metastasis and insulin receptor tyrosine kinase substrate with RAB proteins in the endocytosis of CXCR4.The Journal of biological chemistry · 2019Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The insulin receptor substrate of 53 kDa, IRSp53, is an adaptor protein that works with activated GTPases, Cdc42 and Rac, to modulate actin dynamics and generate membrane protrusions in response to cell signaling. Adult mice that lack IRSp53 fail to regulate synaptic plasticity and exhibit hippocampus-associated learning deficiencies. Here, we show that 60% of IRSp53 null embryos die at mid to late gestation, indicating a vital IRSp53 function in embryonic development. We find that IRSp53 KO embryos displayed pleiotropic phenotypes such as developmental delay, oligodactyly and subcutaneous edema, and died of severely impaired cardiac and placental development. We further show that double knockout of IRSp53 and its closest family member, IRTKS, resulted in exacerbated placental abnormalities, particularly in spongiotrophoblast differentiation and development, giving rise to complete embryonic lethality. Hence, our findings demonstrate a hitherto under-appreciated IRSp53 function in embryonic development, and further establish an essential genetic interaction between IRSp53 and IRTKS in placental formation.
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