Ask about this productRelated genes to: MICAL1 antibody
- Gene:
- MICAL1 NIH gene
- Name:
- microtubule associated monooxygenase, calponin and LIM domain containing 1
- Previous symbol:
- NICAL
- Synonyms:
- MICAL, FLJ11937, DKFZp434B1517, FLJ21739
- Chromosome:
- 6q21
- Locus Type:
- gene with protein product
- Date approved:
- 2003-05-20
- Date modifiied:
- 2016-10-03
Related products to: MICAL1 antibody
Related articles to: MICAL1 antibody
- Molecule Interacting with CasL 1 (MICAL1) is a flavoprotein monooxygenase that promotes filamentous actin (F-actin) depolymerization. Transcriptomic studies have linked MICAL1 downregulation to skeletal muscle atrophy and muscular dystrophy, yet its functional contribution to myogenesis remains unexplored. We found that MICAL1 protein increased progressively during myogenic differentiation of C2C12 cells, reaching a maximum on day 5 in parallel with myosin heavy chain (MyHC). siRNA-mediated MICAL1 silencing produced an ~1.7-fold accumulation of F-actin, while total β-actin protein remained unchanged, indicating a shift in the G-/F-actin equilibrium toward polymerization rather than altered actin expression. The accumulated F-actin reduced YAP1 phosphorylation, promoted its nuclear translocation, and increased the expression of the YAP1 target gene CTGF. MICAL1 depletion also enhanced myoblast proliferation: EdU incorporation and cell viability increased, and PCNA, CCNB1, and CCND1 protein expression was upregulated, while the cell cycle distribution shifted toward the G2/M phase, with a reciprocal loss in G0/G1. Concurrently, MICAL1 knockdown suppressed MyoD, Myogenin, and MyHC throughout differentiation and severely impaired myotube formation, with reductions in the fusion index, myotube area, and length. We conclude that MICAL1 is required for the proliferation-to-differentiation switch in myoblasts and that its activity restrains F-actin-driven YAP1 signaling to permit timely myogenic commitment. MICAL1 may therefore represent a candidate for further investigation in muscle-wasting diseases. - Source: PubMed
Publication date: 2026/07/22
Ngo Thanh Huu PhanLy Quoc KietLee Wan - Copper is essential for cellular function but can become toxic in excess. Although its redox and enzymatic roles are well established, how copper availability affects cytoskeletal organization and cell mechanics remains unclear. Here, we show that elevated copper availability increases membrane tether force and F-actin anisotropy in HK-2 proximal tubule cells, consistent with actin cytoskeletal remodeling. Cotreatment with the membrane-permeable reactive oxygen species (ROS) scavenger Tiron reversed copper-induced ROS accumulation and mechanical changes without affecting cell viability, supporting a ROS-dependent mechanism. Quantitative proteomics and post-translational modification profiling (ProteomeXchange: PXD072220) identified coordinated changes in actin-regulatory proteins, including Rab35, methionine sulfoxide reductase B2, casein kinase 2 subunits, and Septin2, together with reduced actin methionine oxidation and copper-sensitive phosphorylation shifts. These findings identify copper-driven redox signaling as a modulator of renal epithelial cell mechanics associated with remodeling of actin-regulatory pathways. Copper-driven redox signaling remodels the actin cytoskeleton and reprograms the mechanical properties of renal proximal tubule cells. Using optical tweezers, fluorescence imaging, quantitative proteomics, and PTM profiling, we link ROS-dependent mechanical changes to coordinated remodeling of the Rab35/MICAL1/MsrB2 and CK2/Septin2 regulatory axes, establishing copper availability as a modulator of renal epithelial cell mechanics with potential relevance to copper dyshomeostasis in kidney injury. - Source: PubMed
Publication date: 2026/07/21
Pompeu PedroSoares JulianaÁvila Dos Santos ÍrisPinheiro Giuliano MartinsDamasceno Nicole JacintoDomingues Romênia RamosGrelle Glória M R SEinicker-Lamas MarceloPontes BrunoValverde Rafael H F - About 1%-9% of full-term male newborns suffer from cryptorchidism, which is one of the most common congenital abnormalities in the male reproductive tract. Dysregulation of the crosstalk between macrophages and Leydig cells has been implicated in its pathogenesis. However, the mechanisms by which environmental endocrine disruptors disrupt the crosstalk between macrophages and Leydig cells remain insufficiently defined. In this study, it was demonstrated that prenatal exposure to DEHP induces cryptorchidism and defective spermatogenesis in C57BL/6 male offspring, accompanied by marked reductions in Leydig cell quantity, testosterone production and steroidogenic enzyme expression. Notably, Trem2, an immunoregulatory receptor expressed on testicular macrophages, was significantly downregulated following DEHP exposure. Further investigation revealed that MEHP-activated macrophages exacerbate the inhibitory effects of MEHP on Leydig cell proliferation and steroidogenic function. Transcriptomic profiling of macrophages with Trem2 overexpression identified Mical1 as the most significantly upregulated gene. In vitro, MEHP stimulation led to decreased expression of Trem2, Mical1, and Erk in macrophages. Trem2 overexpression restored Mical1 and Erk signaling and Trem2 activation rescued Leydig cell proliferative capacity, while Trem2 silencing further suppressed Mical1 and Erk expression and exacerbated Leydig cell dysfunction. Moreover, Mical1 overexpression reversed the MEHP-induced downregulation of Mical1 and Erk. These findings highlight the Trem2-Mical1-Erk axis as a critical immunoregulatory pathway linking DEHP-induced macrophage activation to testosterone insufficiency. The discovery provides new insights into the etiology of cryptorchidism and identifies potential targets for DEHP-induced cryptorchidism. - Source: PubMed
Publication date: 2026/03/12
Ye SongyiWu ShuangYuan GutongXu JieCai BochengChen JinlingGe Wenliang - Lateral temporal lobe epilepsy (LTLE) is characterized by auditory auras and is often associated with genetic factors. Previous studies have identified various genes linked to LTLE, including . However, there remains a need to explore other genetic variants that contribute to the LTLE phenotype, particularly in the absence of mutations. - Source: PubMed
Publication date: 2026/02/19
Salman BarışKesim YeşimŞirin Nermin GörkemSüsgün SedaUzun Güneş Altıokkaİşeri Sibel UğurBebek NersesBaykan Betül - PURPOSE: Oncogenesis and tumor progression have been linked to abnormal metabolism. We aimed to investigate the potential connection between sulfur metabolism-related genes and clinical features of patients with breast cancer. METHODS: Machine learning algorithms were utilized to assess the risk index of sulfur metabolism-related genes in breast cancer. All patients were categorized into high- and low-risk clusters, based on their calculated average risk scores. Kaplan–Meier curves were used to evaluate the patient prognoses in different groups. Enrichment analysis was performed on the differentially expressed genes (DEGs) across these distinct clusters. The effect of the highest-risk gene, HSPA9, on the malignant behavior of tumor cells was appraised through siRNA transfection. RESULTS: A risk model with nine sulfur metabolism-related genes (ACOT2, ACOT4, CHPF, ELOVL2, HLCS, HSPA9, MICAL1, SPOCK2, and TCF7L2) was established, and low-risk groups exhibited better outcomes than high-risk groups. Various biological functions and pathways of the DEGs were observed between the different groups. The high-risk group exhibited a higher immune cell infiltration rate than the low-risk group. Inhibiting HSPA9 expression effectively reduced breast cancer cell proliferation and migration. CONCLUSION: Our genetic risk model provides a novel pattern for prognostic evaluations and individualized therapeutic strategies for breast cancer. Given its association with breast cancer risk, HSPA9 represents an exceptionally promising therapeutic target. - Source: PubMed
Publication date: 2026/01/16
Yuan YuanZhang ShuyaoFu JialeiZhou Fei