MDFIC antibody
- Known as:
- MDFIC (anti-)
- Catalog number:
- orb101194
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- MDFIC antibody
Related genes to: MDFIC antibody
- 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 antibody
Related articles to: MDFIC antibody
- Coordinated development and homeostasis among bone, muscle, and adipose tissue are essential for the sustainable advancement of the broiler industry. Bone marrow mesenchymal stem cells (BMSCs) possess multi-lineage differentiation potential and provide an in vitro model for investigating regulatory mechanisms of the "bone-muscle-adipose" balance. Nevertheless, microRNA (miRNA)-mRNA regulatory network and the functions of key miRNAs during myogenic differentiation of chicken BMSCs remain unclear. We profiled mRNA and miRNA expression during this process to identify key miRNAs regulating BMSC proliferation and differentiation. mRNA sequencing (mRNA-seq) and miRNA sequencing (miRNA-seq) before and after 5-azacytidine (5-Aza) induction identified 2,233 differentially expressed genes (DEGs) and 67 differentially expressed miRNAs (DE miRNAs). DEGs were mainly enriched in cell cycle and DNA replication pathways, whereas predicted targets of DE miRNAs were predominantly enriched in calcium signaling pathway. A candidate miRNA-mRNA regulatory network was constructed using 13 skeletal muscle-related DE miRNAs and inversely expressed target mRNAs, with target genes enriched in protein processing in the endoplasmic reticulum and Wnt signaling pathways. RNAhybrid prediction and dual-luciferase reporter assays confirmed that miR-26a-5p directly targets MyoD Family Inhibitor Domain Containing (MDFIC). Functionally, miR-26a-5p overexpression suppressed proliferation markers (CCNB2, CCND2, CDK8) and myogenic markers (MYOD1, MYOG, MEF2C, MYHC, Desmin), and reduced MYOD1 protein, whereas miR-26a-5p inhibition produced opposite effects. Collectively, this study delineates the miRNA-mRNA regulatory network during myogenic differentiation of chicken BMSCs and demonstrates that miR-26a-5p negatively regulates proliferation and myogenic differentiation by targeting MDFIC. These findings identify candidate targets for understanding the post-transcriptional regulation of myogenesis in chicken BMSCs. - Source: PubMed
Publication date: 2026/05/25
Liu ShuibingLu YadaWu LinxiQin ZijianZhao ChangbinZhou ZhenSong YongxiangZhang XiquanZhang DexiangLi Hongmei - Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies worldwide, and diabetes mellitus has been recognized as both a risk factor for and a potential consequence of PDAC. However, the epidemiological trends and shared molecular mechanisms underlying this association are not completely understood. - Source: PubMed
Publication date: 2026/05/25
Zhang JiaxiLiu ZhibinHuang KeYi JunkooKim Myoung Ok - Merkel cells are epithelial cells involved in the discrimination of light touch. Situated in the skin, these specialized 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, which 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 in complex with auxiliary subunits MDFIC or MDFI. Moreover, PIEZO1 strongly influences 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 conclusion, utilizing MCC13 cells as a simple in vitro model of native Merkel cell mechanotransduction should be carried out with caution. - Source: PubMed
Publication date: 2026/05/28
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