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
- 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 - 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. - Source: PubMed
Publication date: 2026/01/16
Yuan YuanZhang ShuyaoFu JialeiZhou Fei - Lung cancer (LC) is among the most prevalent cancers globally, posing a significant threat to human health. This study employed Mendelian randomization (MR) analysis to identify key drug targets for LC treatment. MR results from the inverse variance weighted (IVW) algorithm highlighted 352 expression quantitative trait loci (eQTLs) and 31 protein quantitative trait loci (pQTLs) causally associated with LC. Sensitivity and Steiger analyses confirmed that 305 eQTLs and 28 pQTLs exhibited a robust causal relationship with LC. Colocalization analysis further identified 20 eQTLs as potential drug targets for LC. Predictions were made for 257 drugs and 17 diseases, establishing a target-drug network that included PTGFR-D005557 and IREB2-C004925, among others. The drugs-diseases network revealed associations such as D007213 with Liver Cirrhosis and D013749 with Schizophrenia. Notably, the strongest binding interaction was observed between Valproic acid and eight genes (BRAT1, H2BC11, IREB2, MICAL1, MPHOSPH6, PTGFR, RHNO1, SERPING1), suggesting a significant molecular interaction. Ultimately, seven key drug targets (SERPING1, TDRD9, GBAP1, FAM241A, ZKSCAN4, ZKSCAN3, Z94721.1) were consistently identified across two MR studies and validated. These targets offer new avenues for LC treatment, highlighting their potential in therapeutic development. - Source: PubMed
Publication date: 2025/12/23
Huang YaweiGeng MengyaZhang Mukun - NADPH oxidase organizer 1 (NoxO1) is known as a scaffold cytoplasmic subunit of the reactive oxygen species (ROS) forming Nox1 complex. We previously identified an interaction between NoxO1 and Erbin, a cytosolic scaffold protein that associates with Epidermal Growth Factor Receptor (EGFR), but its ROS-independent roles remain poorly understood. Here, we demonstrate that NoxO1 overexpression remodels the endolysosomal system by expanding early endosomes and lysosomes. A calibrated six-compartment ordinary differential equation model of EGFR trafficking predicts a slowed down intracellular trafficking: NoxO1 overexpression increased internalization rates by 14 % while reducing degradative sorting by 48 %, lysosomal transfer by 24 %, and final degradation by 41 %. Using fluorescent cargo (EGF and BSA), we confirmed enhanced internalization and cargo accumulation in lysosomes, supporting the idea of prolonged lysosomal retention in NoxO1 overexpressing cells. Mechanistically, NoxO1 activated transcription factor EB (TFEB), the master regulator of lysosomal biogenesis, in an Erbin-dependent but ROS independent manner. Proximity ligation assays revealed spatial association of NoxO1, Erbin, EGFR, and TFEB, suggesting a multi-protein regulatory complex. Genetic ablation of Erbin abolished NoxO1-induced increases in early endosome (EEA1) and lysosome (LAMP1) markers, confirming Erbin's essential role. In conclusion, via its interaction with Erbin NoxO1 promotes activation of TFEB, contributes to lysosome formation while delaying cargo degradation. - Source: PubMed
Publication date: 2025/12/12
Hebchen MaureenHerwig FalkSchader TimSpaeth ManuelaMüller NiklasSchröder Katrin