MESP1 antibody - C-terminal region (ARP35960_P050)
- Known as:
- MESP1 (anti-) - C-terminal region (ARP35960_P050)
- Catalog number:
- arp35960_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- MESP1 antibody - C-terminal region (ARP35960_P050)
Related genes to: MESP1 antibody - C-terminal region (ARP35960_P050)
- Gene:
- MESP1 NIH gene
- Name:
- mesoderm posterior bHLH transcription factor 1
- Previous symbol:
- -
- Synonyms:
- MGC10676, bHLHc5
- Chromosome:
- 15q26.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-10-21
- Date modifiied:
- 2015-06-16
Related products to: MESP1 antibody - C-terminal region (ARP35960_P050)
Related articles to: MESP1 antibody - C-terminal region (ARP35960_P050)
- Endochondral ossification is a physiological process involving a sequential formation of cartilage and bone tissues. Classically, cartilage and bone formation have been considered independent processes at cellular level. However, the recently described multiple cell differentiation dynamics suggest that some bone cells are indeed the progeny of cartilage cells, or chondrocyte-derived osteoblasts. We hypothesized that the cartilage-to-bone phenotype transition is triggered by specific molecular events. First, the process was assessed in mouse bone tissue, and then, it was mimicked using in vivo cell implantation and in vitro serial differentiation protocols. Data indicates that cartilage cells transition to bone cell phenotype during postnatal physiological bone formation. This process can be reproduced using cartilage precursor cells coupled to specific implantation procedures or differentiation protocols. Gene expression profiling reveals that NOTCH, BMP and MAPK signaling pathways are relevant at the phenotype-switch, while the transcription factors Mesp1, Alx1, Grhl3 and Hmx3 are the feasible driver genes for chondrocyte-derived osteoblasts formation. Altogether, this report shows that endochondral ossification can be modeled using primary cell cultures and data indicate that this process is regulated by specific molecular events, previously described at skeleton morphogenesis during embryo development, and from now on also linkable to postnatal bone development and regeneration processes. - Source: PubMed
Publication date: 2026/02/09
Ruiz-Hernández RaquelGay LaurieMoncho-Amor VerónicaMartín PabloVergara-Arce Jhonatan ADi Blasio StefaniaSnoeks ThomasCossío UnaiMatheu AnderCaffarel Maria MGerovska DanielaAraúzo-Bravo Marcos JVilas AmaiaProsper FelipeMoya SergioAlonso-Alconada DanielAlonso-Varona AnaNusspaumer GretelLopez-Rios JavierRizotti KarineLovell-Badge RobinBonnet DominiqueMalanchi IlariaAbarrategi Ander - Non-small cell lung cancer (NSCLC) remains a leading cause of cancer-related deaths worldwide, necessitating the identification of novel therapeutic targets. Mesoderm posterior bHLH transcription factor 1 (MESP1) has been implicated in various developmental processes, but its role in cancer, particularly NSCLC, is poorly understood. Given the emerging evidence linking MESP1 to cellular processes relevant to cancer biology, investigating its regulatory mechanisms in NSCLC could provide critical insights for developing new therapies. This study employed quantitative real-time PCR (qRT-PCR) to assess the mRNA levels of MESP1, ubiquitin specific peptidase 7 (USP7), and clusters of differentiation 163 (CD163). Western blotting was used to analyze the protein expression of MESP1 and USP7. Cellular proliferation was evaluated through colony-forming assays, while apoptosis was quantified using flow cytometry. Mitochondrial membrane potential was measured by JC-1 staining, and reactive oxygen species (ROS) levels were also analyzed via flow cytometry. Additionally, colorimetric assays were utilized to determine malondialdehyde (MDA), total iron, and Fe levels. The in vivo effects of MESP1 silencing on NSCLC progression were examined using a xenograft mouse model. GST-pull down assay, Co-immunoprecipitation (Co-IP) assay, and ubiquitination assay were conducted to explore the interaction between USP7 and MESP1. The expression of both MESP1 and USP7 was found to be upregulated in NSCLC tissues and cells when compared with normal lung tissues and normal human bronchial epithelial cells. Knockdown of MESP1 significantly inhibited NSCLC cell proliferation, induced apoptosis and promoted features associated with ferroptosis. Moreover, MESP1 silencing suppressed M2 macrophage polarization and tumor formation. Mechanistically, USP7 was identified to stabilize MESP1 protein expression through its deubiquitinating activity. Overexpression of MESP1 attenuated the inhibitory effects of USP7 silencing on NSCLC cell proliferation and M2 macrophage polarization and also mitigated the promoting effects of USP7 knockdown on apoptosis and the induction of features associated with ferroptosis. USP7 stabilized MESP1 to promote the malignant progression of NSCLC. The findings highlight the potential of targeting the USP7-MESP1 axis as a novel therapeutic strategy for NSCLC. - Source: PubMed
Publication date: 2026/01/21
Jiang ShashaRong LiwenYi FeiYang PengYang Longjing - Stem cell therapeutics is an area of active investigation for the treatment of cardiovascular disease. Unlike adults, neonatal hearts possess unique regenerative capacity immediately after birth, suggesting that neonatal cardiovascular tissue may be a promising and untapped resource of stem cells. In the current study, we present the unique transcriptome and differentiation capability of neonatal + + + stem cell clones isolated from humans. Comparable + + + stem cell clones were then isolated from sheep for functional analysis in a sheep model of myocardial infarction and allogeneic stem cell-based repair without immunosuppression. - Source: PubMed
Publication date: 2026/01/05
Hughes LoreleiBaio JonathanHasaniya NahidhBailey LeonardKim JuliaYanez DanielleAustin EdwardVega RichardRivera Morales PaolaCamberos VictorWilson Christopher GVeliz Alicia LKearns-Jonker Mary - Functional single ventricle (FSV) comprises a heterogeneous group of congenital heart diseases (CHDs) with severe and complex abnormalities. The multifactorial etiology of the disease poses challenges in identifying specific pathogenic factors and planning effective interventions and preventive treatments for patients. Whole-exome sequencing (WES) was performed to identify variants in relevant genes in 29 FSV patients from different families. In total, 95 heterozygous variants across 48 CHD-associated genes were identified, including 85 missense, four small indel, one splicing, one stop gain, and four synonymous variants. Among them, 22 were novels, 11 conflicting, and four pathogenic variants. Each patient carried from two to six variants in different genes, including at least one variant in genes associated with serious heart defects such as , , , , , , , , , , , , , , and . In addition, the variants in the , , , , , , , , , and genes are associated with characteristic phenotypes of FSV, such as atrial septal defect, ventricular septal defect, small left heart syndrome, transposition of the great arteries, and double outlet right ventricle occurring at high frequency in patients. The prediction results suggest that these are potentially pathogenic variants in patients and may explain the phenotype in patients. This is the first study to identify variants associated with functional single ventricle, a complex form of congenital heart disease. Our results contribute to a general understanding of the causes of the disease, thereby guiding treatment and prevention approaches for patients. - Source: PubMed
Publication date: 2025/10/17
Tu Le TrongLien Nguyen Thi KimTung Nguyen VanVan Dang Thi HaiNga Vu QuynhTho Nguyen TatHien Nguyen ThanhDuc Nguyen MinhHoang Nguyen Huy - Congenital heart disease (CHD) is the most common birth defect and involves intricate developmental mechanisms. Uric acid (UA), the final metabolite of purine degradation in humans, has a largely unexplored role in heart development. This study investigated the effects of elevated UA levels-both exogenous and endogenous-on cardiac development in a zebrafish model and explored the involvement of Wnt signaling in this process. UA elevation was achieved through exogenous UA exposure, in vivo overexpression of xdh, and knockdown of uox. Expression levels of Wnt pathway components (wnt1, wnt3a, wnt6b, and β-catenin), cardiac progenitor markers (mesp1 and isl1), neural crest cell markers (sox10 and crestin), and cardiac development genes (nkx2.5, tbx5a, and fgf10a) were assessed at key developmental stages. All UA-elevating strategies significantly increased UA concentrations and led to phenotypes including pericardial edema and reduced heart rate at 72 h post-fertilization (hpf). These phenotypes were accompanied by downregulation of Wnt signaling and cardiac development genes. Treatment with the Wnt activator CHIR99021 partially rescued the cardiac defects induced by UA overload. These findings demonstrate that elevated UA-whether exogenous or endogenous-can disrupt cardiac development in zebrafish, at least in part by suppressing Wnt signaling, thereby impairing downstream gene networks essential for heart morphogenesis. - Source: PubMed
Publication date: 2025/08/21
Li YahongYang PeiyingWang XinZhang ZhileiJiang TaoSun YunXu Zhengfeng