Ask about this productRelated genes to: MYH9 antibody
- Gene:
- MYH9 NIH gene
- Name:
- myosin heavy chain 9
- Previous symbol:
- DFNA17
- Synonyms:
- NMMHCA, NMHC-II-A, MHA, FTNS, EPSTS
- Chromosome:
- 22q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-03-12
- Date modifiied:
- 2019-04-23
Related products to: MYH9 antibody
Related articles to: MYH9 antibody
- Extracellular vesicles (EVs) are promising to provide chemical predictors toward clinical diagnosis and prognosis. However, the isolation of high-purity EVs from complex bodily fluids is a little complex. To address this issue, a choline phosphate (CP)-functionalized adsorbent, designated as SCF@CP-Et, was prepared by grafting 2-(isopropylacryloyloxy)ethyl choline phosphate (CP-Et) from the surface of sulphydryl cotton fiber (SCF) via thiol-ene click polymerization. The SCF@CP-Et indicates a high-efficiency EV enrichment capability arising from the multivalent coordination interaction between the CP groups and phosphatidylcholine (PC) on EV membrane surface, meanwhile possesses an excellent anti-protein adsorption performance derived from the abundant hydroxyl groups of cotton fiber and zwitterionic property of CP-Et. Besides, this cotton fiber is easily assembled into a cotton fiber-in-syringe solid-phase extraction (SPE) device. This device shows simple and convenient operation during the isolation of EVs from various samples, including cell culture medium, plasma and urine. Meanwhile, the released EVs can maintain their biological activity. Taking advantage of these properties, this method was employed to isolate EVs in the plasma of colorectal cancer (CRC) patients and healthy donors, and 69 up-regulated and 18 down-regulated proteins are identified by proteomics analysis. Most of these up-regulated proteins, such as TLNA, FLNA, ITGB3 and MYH9, are associated with the progression of CRC, demonstrating the potential of this carbon fiber-based SPE method in the EV-based early diagnosis of diseases. - Source: PubMed
Publication date: 2026/04/17
Chen MengxiTang YingyingJiang ZiyiZhang JingZhang HaiyangWei Yinmao - Growth factors selectively activate calcium signaling pathways in the cell nucleus, which in turn regulate gene transcription and other intranuclear events, but the specific way this is accomplished is not entirely understood. Growth factors increase inositol 1,4,5-trisphosphate (IP3) in the nucleus, which in turn releases calcium from intranuclear IP3 receptors (ITPRs), and the present study shows that this leads to transient assembly of an actin nucleoskeleton that associates with intranuclear non-muscle myosin 2A (MYH9). Mass spectrometry suggests that much of the MYH9 cargo consists of components of the gene transcription machinery, and chromatin immunoprecipitation identified a number of specific genes that associate with the myosin in response to stimulation with growth factors. Together, these findings suggest that growth factors initiate gene transcription by transiently assembling an actin nucleoskeleton that works with MYH9 to bring specific genes to the transcription machinery. - Source: PubMed
Publication date: 2026/05/06
González María JoséRodrigues Michele AngelaDiprima SantoZhao DejianBassani Thais FernandesFernandez Clara CoutoKruglov EmmaNathanson Michael HGomes Dawidson Assis - Deoxyribonuclease 1 Like 3 (DNASE1L3) is a member of the deoxyribonuclease I family that is associated with some diseases, including systemic lupus erythematosus and hypocomplementemic urticarial vasculitis. Recently, abnormal DNASE1L3 was preliminarily shown to correlate with tumor pathogenesis. However, its role is still undetermined in nasopharyngeal carcinoma (NPC). - Source: PubMed
Publication date: 2026/05/06
Tao XingyuLiu XiongZhao XiangdongZhou BeixianCheng ChaoYan WeiweiHe JingjingCao HaolinSu YunXin JianyangGan XiaoningPeng HongLin WanliFang WeiyiLiu Zhen - Acute pancreatitis is a systemic inflammatory response that has the potential to affect numerous organs, resulting in persistent multiorgan failure and necrosis of the pancreas. According to previous studies, the development and occurrence of acute pancreatitis are linked to ferroptosis and immune responses. We assessed and validated the function of ferroptosis-related genes in acute pancreatitis and their association with inferred immune infiltration using bioinformatic analyses. Ferroptosis-related differentially expressed genes were identified using the Gene Expression Omnibus databases (GSE109227, GSE121038, and GSE183158) in conjunction with our transcriptome sequencing data. The involvement of ferroptosis-related differentially expressed genes was clarified through gene ontology, differential gene correlation, and gene set enrichment analysis. CIBERSORT analysis was used to evaluate and internally validate the immune microenvironment in acute pancreatitis. Comparative analysis of sequencing data from the pancreatic and liver tissues revealed 13 ferroptosis-related differentially expressed genes in acute pancreatitis. Gene ontology analysis primarily identified enrichment for iron ions, protein phosphatase, and actin filament binding. Gene set enrichment analysis predominantly highlighted the interleukin-18 and interleukin-23 pathways. Hub genes in the protein-protein interaction network included Egfr, Fads1, Hsp90b1, Krt18, Lcn2, Myh9, Pdia6, and Sqle. We identified 80 miRNAs, 67 transcription factors, and 24 potential drugs or molecular compounds associated with acute pancreatitis pathology. Quantitative reverse transcription polymerase chain reaction performed on caerulein-induced acute pancreatitis mouse models confirmed significant downregulation of Fads1, Hsp90b1, Pdia6, Sqle, and Cisd1 mRNA levels while showing significant upregulation of Osbpl9, Myh9, and Zfp36 mRNA levels. These findings suggested that these genes may represent candidate genes associated with AP and ferroptosis. Thirteen ferroptosis-related differentially expressed genes were discovered within the framework of acute pancreatitis, and their association with immune cell infiltration was studied. Future investigations should explore the possibility of Fads1, Hsp90b1, Pdia6, Sqle, Cisd1, Osbpl9, Myh9, and Zfp36 as novel therapeutic targets. - Source: PubMed
Publication date: 2026/04/29
Liu HuiYue MengliChen ShangsiLiu Pi - Neutrophil migration to bacterial infection sites is key for host defense. Host ribosomal protein SA (RPSA) has been recently reported to regulate the anti-infection immunity of immune cells; however, its role in neutrophil migration remains unclear. Here, using myeloid-specific Rpsa-deficient mice, we found that RPSA deletion inhibited neutrophil infiltration and markedly exacerbated Streptococcus suis serotype 2 infection. Adoptive cell transfer and neutrophil depletion assays identified RPSA as vital for the anti-infective function of neutrophils. Mechanistically, RPSA deficiency induced the overexpression of olfactomedin 4 (OLFM4), which in turn inhibited the activation of the RhoA/ROCK1/pMLC2 signaling pathway, reduced MYH9 expression, and caused aberrant MYH9 translocation from the uropod to the cytosol in migrating neutrophils. Ultimately, this disrupted cytoskeletal polarization and uropod extension, thereby abrogating migratory function. Clinically, septic patients' neutrophils exhibited reduced RPSA and elevated OLFM4 expression, a phenotype that correlated with a marked impairment of migratory capacity. Therapeutic targeting of the RPSA-OLFM4 axis restored neutrophil migration and improved disease outcomes in both S. suis 2-infected and septic mice. Thus, our findings demonstrate that RPSA promotes neutrophil migration via downregulating OLFM4 to counter bacterial infection, and establish the RPSA-OLFM4 axis as a critical immune migratory checkpoint in host antibacterial immunity. - Source: PubMed
Publication date: 2026/04/25
Wu TongYang XiangruiLei SiyuWei ShaopengWang WeiSun YiJiang HexiangJia XiuwenTian YanyanZhang KaixinZhang YufanChen HaizhenHuang JingLi FengyangLi NaLei Liancheng