ArticleBiochemical Society transactions2023
SPECC1L: a cytoskeletal protein that regulates embryonic tissue dynamics.
Article in Biochemical Society transactions, 2023. 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, 10 citations in OpenAlex.
- Ectodermal loss of ARHGAP29 alters epithelial morphology and disrupts murine palatogenesis.Development (Cambridge, England) · 2026Article
- Perioperative Care of a Four-Year-Old Child With Teebi Hypertelorism Syndrome: A Rare Craniofacial Disorder.Journal of medical cases · 2026Article
- Loss of SPECC1L in cranial neural crest cells results in increased hedgehog signaling and frontonasal dysplasia.Frontiers in physiology · 2026Article
- Loss of SPECC1L in cranial neural crest cells results in increased hedgehog signaling and frontonasal dysplasia.bioRxiv : the preprint server for biology · 2025Article
- Genetic interaction ofbioRxiv : the preprint server for biology · 2025Article
- Disruption of SPECC1L translation initiation by intragenic deletion: novel pathogenic mechanism in Teebi-hypertelorism syndrome.NPJ genomic medicine · 2025Article
- Review
- Case Report: Dual resistance to dasatinib/olverembatinib in accelerated-phase cml: identification of a novelFrontiers in oncology · 2025Article
- Novel insights into palatal shelf elevation dynamics in normal mouse embryos.Frontiers in cell and developmental biology · 2025Article
- NTRK-rearranged spindle cell tumor with SPECC1L-NTRK3 fusion in the thoracic spine: a case report.Journal of cancer research and clinical oncology · 2024Article
- Proteus syndrome with progressive paralysis of the unilateral lower limb: A rare case report and literature review.Heliyon · 2024Article
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
Many structural birth defects occur due to failure of tissue movement and fusion events during embryogenesis. Examples of such birth defects include failure of closure of the neural tube, palate, and ventral body wall. Actomyosin forces play a pivotal role in these closure processes, making proteins that regulate actomyosin dynamics a priority when studying the etiology of structural birth defects. SPECC1L (sperm antigen with calponin homology and coiled-coil domains 1 like) cytoskeletal protein associates with microtubules, filamentous actin, non-muscle myosin II (NMII), as well as membrane-associated components of adherens junctions. Patients with SPECC1L mutations show a range of structural birth defects affecting craniofacial development (hypertelorism, cleft palate), ventral body wall (omphalocele), and internal organs (diaphragmatic hernia, bicornuate uterus). Characterization of mouse models indicates that these syndromic mutations utilize a gain-of-function mechanism to affect intra- and supra-cellular actin organization. Interestingly, SPECC1L deficiency appears to affect the efficiency of tissue dynamics, making it an important cytoskeletal regulator to study tissue movement and fusion events during embryonic development. Here we summarize the SPECC1L-related syndrome mutations, phenotypes of Specc1l mouse models, and cellular functions of SPECC1L that highlight how it may regulate embryonic tissue dynamics.
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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 Socratic graph.