Ask about this productRelated genes to: CRYM antibody
- Gene:
- CRYM NIH gene
- Name:
- crystallin mu
- Previous symbol:
- -
- Synonyms:
- DFNA40
- Chromosome:
- 16p12.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-26
- Date modifiied:
- 2015-11-12
Related products to: CRYM antibody
Related articles to: CRYM antibody
- - Source: PubMed
Publication date: 2026/04/13
Xu YanZhao PanpanYao ZhipengShen TianxiaoDing ShaodongHua YunpengZhang FanJiang XiaochunDi GuangfuXia Hongping - Research shows that patients with viral pneumonia complicated by diabetes have a worse prognosis and higher mortality. Our study aimed to assess the effect of diabetes on respiratory tract microbes and the transcriptome in patients with viral pneumonia. We included 76 subjects from China-Japan Friendship Hospital, including 16 healthy people, 17 patients with viral pneumonia and diabetes (VD), and 43 patients with viral pneumonia without diabetes (VP). We collected their sputum samples for both metagenomic and 16S rRNA sequencing and collected blood samples for RNA sequencing. In transcriptome analysis, the VD group downregulated the expression of PTCH1 and upregulated the expression of ANK1, RBM38, BPGM, CRYM, TAL1, and HBD. The differential pathways are mainly reflected in the formation, development, and maintenance of red blood cells, the activity of immunoglobulins, and the membrane transport and transportation of substances. There is a significant difference in microbial diversity between the two groups. Both analysis methods demonstrate a significant increase in the abundance of , and in the VP group. The host genes AGAP1, RNF182, and ANKRD9 are particularly closely associated with microorganisms. Our results suggest that diabetes may inhibit the expression of genes related to immune regulation, energy metabolism, and oxygen utilization in patients with viral pneumonia. Meanwhile, we predict that VD may be associated with a decrease in microbial diversity and a decline in microbial functions in cellular processes, environmental adaptation, metabolism, and genetic activity. These abnormalities can worsen the course of viral pneumonia and affect the prognosis of patients. - Source: PubMed
Publication date: 2026/04/06
Huang ChangruiFeng QinqiYu BangZou HaoCai YashiLiu JianLi DeminZhang HongchunZou Xiaohui - Differentiated human neuroblastoma (SH-SY5Y) cells were exposed to either 0.2 μM nicotine, a tobacco smoke preparation (TPM) diluted to the same nicotine concentration, or a cocktail of seven tobacco smoke monoamine oxidase inhibitors (MAOIs) at the concentrations measured in the TPM. Treatment occurred for 3 days, such that the cellular monoamine oxidase (MAO) concentration was reduced by approximately 50% in both the TPM and MAOI cocktail exposure groups. Changes in gene expression after exposure to the different treatments were determined using qPCR, and the effect of these exposure treatments on global gene expression was also examined using mRNA sequencing. No change in and gene expression levels was observed, after any treatment, either using qPCR or mRNA sequencing. The MAOI versus control treatment comparison revealed that four genes were >2-fold down-regulated (, , , ), and 19 genes were up-regulated after 3 days' exposure to the MAOI cocktail. Many of these differentially expressed genes were linked with disease conditions related to smoking and addiction. Exposure to nicotine and TPM each resulted in up- and down-regulation of different sets of genes. The results indicate that changes in MAO gene expression are unlikely to be responsible for the changes in MAO activity. The association between genes whose expression changes with tobacco MAO treatment and smoking-related diseases and addiction suggests the central role that MAO inhibition may play in mediating the effects of smoking on smokers. - Source: PubMed
Publication date: 2026/02/09
Niraula PrakshitPage Rachel APalmer Barry RTruman Penelope - Male CD-1 mice form linear social hierarchies and can rapidly reform them following social reorganization. Through tag-based sequencing in the medial amygdala (MeA), we identified several genes regulating cholinergic signaling, myelination, and thyroid signaling that rapidly shift expression 70 min after animals change social status. Here, we further characterize the expression patterns of individual genes within these pathways in both stable and reorganized hierarchies. We find that genes related to cholinergic signaling show higher expression in the MeA of dominant males in stable hierarchies as well as when reestablishing dominance in reorganized hierarchies. Dominant males also show higher levels of myelination-related genes than socially descending males when reestablishing their social status during social reorganization but less so in stable groups. Conversely, thyroid signaling genes show higher expression in the MeA in subordinate males and previously dominant males who are socially descending. Using RNAscope, we were able to demonstrate broadly similar patterns of gene expression immediately following social reorganization across the MeA, basolateral, and central amygdala for seven genes of interest (chat, slc5a7, ache, mbp, mog, crym, and mybpc1). High levels of coexpression of cholinergic signaling and myelination gene expression in dominant males suggest that these processes work together to promote resilience to the social challenge and promote dominance. In summary, we demonstrate that rapid changes in amygdala gene expression in each pathway are associated with the formation and maintenance of dominance and subordinate social status in stable and reorganized environments. - Source: PubMed
Milewski Tyler MLee WonRada Köll RCurley James P - Thyroid hormone (TH) signaling plays a major role in the development, energy homeostasis, and metabolism of most tissues. Recent studies have identified THs as drivers of prostate cancer (PCa) development and progression. We reported that the T3-scavenger protein µ-crystallin (CRYM) regulates the development and progression of PCa and that this involved crosstalk with androgen receptor (AR) signaling. However, the mechanisms remain incompletely understood. Here, we explored the role of thyroid hormone receptor β (TRβ), which is the main effector of TH signaling, in the context of PCa. The use of the TRβ-selective antagonist NH-3 inhibited PCa cell proliferation in vitro and reduced tumor size in PCa xenograft models in vivo. Notably, NH-3 was highly effective in the engrafted 22Rv1 cell line, a model for castration-resistant PCa (CRPC). Mechanistic studies revealed that NH-3 downregulates AR and the AR target genes Nkx3.1 and KLK3 (PSA). NH-3 was a more effective anticancer agent than enzalutamide, and their combined use was synergistic. Evidence from human datasets corroborates our findings, whereby elevated TRβ expression and mutations in the TH signaling pathway are associated with the onset of PCa. Collectively, these results establish TRβ as a mediator of tumorigenesis in PCa and identify NH-3 as a promising therapeutic agent for targeting AR signaling, particularly in CRPC. - Source: PubMed
Publication date: 2025/10/14
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