Ask about this productRelated genes to: MDFIC Blocking Peptide
- Gene:
- MDFIC NIH gene
- Name:
- MyoD family inhibitor domain containing
- Previous symbol:
- -
- Synonyms:
- HIC, MDFIC1
- Chromosome:
- 7q31.1-q31.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-22
- Date modifiied:
- 2018-02-13
Related products to: MDFIC Blocking Peptide
Related articles to: MDFIC Blocking Peptide
- Merkel cells are epithelial cells involved in the discrimination of light touch. Situated in the skin, these specialised cells decode mechanical cues through the mechanosensitive ion channel PIEZO2. Merkel cell carcinoma lines have been widely used as in vitro models for Merkel cells and like the native cell, they exhibit mechanically evoked currents. Herein, we show that unlike the native Merkel cell, that principally uses PIEZO2, mechanically evoked currents in the Merkel cell carcinoma line MCC13 are predominantly carried by PIEZO1, with variable contributions from PIEZO2. Slowly inactivating current types in these cells are carried by PIEZO1 complexed with auxiliary subunits MDFIC or MDFI. Moreover, PIEZO1 strongly influenced the endogenous levels of MDFIC, a known transcriptional repressor, whereby the loss of PIEZO1 dramatically reduced cellular levels of MDFIC. This suggests that the removal of PIEZO1 from a cell will likely have influences on the cellular transcriptome beyond its canonical Ca2+-based signalling pathways. In summary, utilizing MCC13 as a simple in vitro model of native Merkel cell mechanotransduction should be carried out with caution. - Source: PubMed
Publication date: 2026/05/05
Zhou ZijingPaz-López SoniaKuck LennartVásquez ValeriaCox Charles D - PIEZO channels are critical for sensory mechanotransduction. While MyoD-family inhibitor proteins were identified as PIEZO1 auxiliary subunits, their broader regulatory roles, particularly in sensory cells, remained unclear. Here, we demonstrate native MDFIC and MDFI regulate endogenous PIEZO channel currents in various nonsensory cell types. However, neither MDFIC nor MDFI are expressed in primary sensory neurons. In these cell types, we identified an uncharacterized third member of this family, /, that shares the ability to physically bind to PIEZO1 and PIEZO2. MDFIC2 is selectively expressed in subsets of mechanosensitive neurons, including dorsal root ganglia, trigeminal ganglia, and vagal sensory neurons. Like its paralogues, MDFIC2 alters PIEZO1/2 mechanosensitivity and inactivation kinetics, converting them into high-threshold slowly inactivating mechanoreceptors. Extensive cryo-EM reveals a conserved binding pocket for these auxiliary subunits in the pore modules of both PIEZO1 and PIEZO2 mediated by the posttranslationally modified distal C termini of MyoD-family inhibitor proteins. This structural and functional characterization of MyoD-family inhibitor proteins as PIEZO1/2 channel auxiliary subunits offers insights into the mechanobiology of nonsensory and sensory cells. - Source: PubMed
Publication date: 2026/04/09
Zhou ZijingDai FeiCheng DelfineMa XiaonuoOmidkhoda Seyedeh FarzanehClarke JackZhang HuijingLaden MichaelGuo YangLi Jinyuan VeroLiu RenjingWong Emily SZhang YixiaoCox Charles D - Attention-deficit/hyperactivity disorder (ADHD) is a common heritable neurodevelopmental disorder, affecting ~7 million children (11.4%) in the U.S. However, ADHD's underlying genetic architecture remains largely unknown. Transcriptome-wide association studies (TWAS), which integrate expression quantitative trait loci (eQTL) and GWAS summary data, can identify differentially expressed risk genes underlying complex phenotypes. Here we conduct a TWAS of ADHD using expression data from multiple brain tissues to improve understanding of the complex genetic architecture underlying this psychopathology. - Source: PubMed
Publication date: 2026/02/22
Abrishamcar SarinaDai QileYang JingjingHüls AnkeEpstein Michael P - The gene encodes connexin 37 or Gap junction protein alpha-4. Gap junction proteins are required for lymphatic valvulogenesis. It is known that homozygous knockout of the Gja4 gene in mice leads to lymphatic system dysfunction and absent venous valves. In this report, we identify for the first time a homozygous nonsense variant in the gene, c.97delC (transcript ID NM_002060.3) or p.Arg33Alafs*98, or chr1:g.34794309delC (GRCh38 format) in a human fetus with increased nuchal fold thickness and abnormal fetal ductus venosus termination. Asymptomatic parents were carriers of the same variant. Additionally, a search of the literature showed that this specific variant in the gene has not been previously documented as a cause of human fetal disease. A STRING (Search Tool for Retrieval of Interacting Genes/Proteins) database analysis showed close interactions between the gene and other genes involved in the causation of hereditary lymphedema: and . However, STRING database analysis also showed no interaction of the gene with genes in the rasopathy pathway, which can also be causative of increased fetal nuchal translucency, namely and . Thus, we describe a novel gene-human fetal phenotype association. - Source: PubMed
Publication date: 2025/11/17
Chauhan BinodiniPrajapati Nilamben ASagarkar SnehaMenon PramilaKachhadiya TusharVaniawala ShalinVaniawala SalilTamhankar VasundharaTamhankar Parag M - PIEZO channels are mechanical force sensors involved in various biological processes, including somatosensation. To date, only a few PIEZO-binding partners have been identified, including MyoD-family inhibitor proteins (MDFI and MDFIC). Here, we show that MDFIC2, a third member of the MDFI protein family with an as-yet-unknown function, is expressed in a subset of nociceptive sensory neurons. MDFIC2 modulates both PIEZO1 and PIEZO2 gating properties by slowing their kinetics and shifting mechanical sensitivity to higher forces. Interestingly, is downregulated in mouse neuropathic pain models in which mechanical allodynia is a hallmark symptom. We found that intrathecal administration of adeno-associated virus vector encoding cDNA reduces mechanical sensitivity and attenuates mechanical allodynia in the spared nerve injury neuropathic pain model. These findings demonstrate a mechanism for regulating mechanosensation and highlight a potential therapeutic route for treating mechanical allodynia. - Source: PubMed
Publication date: 2025/11/07
Habib Abdella MLi ShengnanZhang ChenjingJi MeijunOsorio NancyPenalba VirginieTorres Jesus MGossage Samuel JRezai Mehdi AGeard Amy FRahim Ahad AMahmoud Ahmed M MSantana-Varela SoniaZhou JunZhao JingWood John NOkorokov Andrei LZhou XuelongCox James JCoste Bertrand