ZNF537 antibody - middle region (ARP32963_P050)
- Known as:
- ZNF537 (anti-) - middle region (ARP32963_P050)
- Catalog number:
- arp32963_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ZNF537 antibody - middle region (ARP32963_P050)
Related genes to: ZNF537 antibody - middle region (ARP32963_P050)
- Gene:
- TSHZ3 NIH gene
- Name:
- teashirt zinc finger homeobox 3
- Previous symbol:
- ZNF537
- Synonyms:
- KIAA1474, TSH3
- Chromosome:
- 19q12
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-10
- Date modifiied:
- 2016-10-05
Related products to: ZNF537 antibody - middle region (ARP32963_P050)
Related articles to: ZNF537 antibody - middle region (ARP32963_P050)
- This study aimed to elucidate the role of parthanatos-related genes (PRGs) in papillary thyroid carcinoma (PTC) and construct a prognostic risk model to guide personalized treatment. - Source: PubMed
Publication date: 2025/12/02
Wang RuiZhang LiWen Shuxin - Discovering new and viable therapies for genetic diseases is a time-consuming and cost-intensive process, especially for rare disorders. In this study, we highlight how a high-throughput drug discovery platform was utilized to uncover drugs at scale that normalized the signature for a rare neurological neurodevelopmental disease, 19q12 autism spectrum disorder (ASD) associated with deficiencies in ZNF536 and TSHZ3. We first identified the transcriptomic fingerprint of the disease in an in vitro disease model in the form of dysregulated pathways. Subsequently, we measured the biological impact of small molecule drugs in a relevant wild-type cell line and uncovered an approved drug Entrectinib that induced the opposite effect to that in the disease fingerprint, demonstrating the capability to normalize the disease fingerprint. Entrectinib was further prescribed off-label to the identified patient with 19q12 and drug effect was characterized both from blood collection and neuropsychological assessments. Biomarkers from blood recapitulated Entrectinib's pharmacodynamic effect and normalized the disease signature. We show how generation of transferrable transcriptomics-derived disease signatures allows for measuring drug effects on a signature in related wild-type cell lines, making the screen universally applicable and reducing the need for expensive screens in disease models. - Source: PubMed
Publication date: 2025/11/25
Guin DrishtiHaditsch UrsulaBellucci Joseph JTopka SabineDyer Katherine EDel Toro Gabriel A RiveraBlanco Michael RDowns Natalie FPerfito NicoleMahadevan ArunMoxham Christopher M - One of the main challenges in Type 1 diabetes mellitus (T1DM) research is the sample size of the participants and the invasive process of collecting an adequate number of blood samples from young patients with T1DM. Therefore, it is of great interest to investigate the possibility of using saliva as a non-invasive tool to investigate the genetic factors that are associated with T1DM comorbidities. The present study aims to identify differentially expressed genes (DEGs) in saliva samples of T1DM patients with various comorbidities using transcriptomic profiling. - Source: PubMed
Publication date: 2025/10/10
Mussa Bashair MSrivastava AnkitaRajan ReejaVenkatachalam ThenmozhiAl-Habshi AbeerAbdelgadir ElaminBashier AlaaeldinAl Awadi FatheyaHafidh KhadijaHamoudi RifatAbusnana Salah - Anatomic location of white adipose tissue is a determinant of cardiometabolic risk. To understand differences within/between adipose depots, we generated 65,668 single-nucleus transcriptomes from human subcutaneous or intraabdominal adipose tissue (SAT/IAT). Unsupervised analysis revealed 26 adipose-resident cell clusters including two subpopulations of mature adipocytes, characterized by high vs. low expression of adipocyte maturation genes (ADIPOMAT vs. ADIPOMAT ). ADIPOMAT adipocytes demonstrate a low-differentiation, pro-inflammatory, and pro-fibrotic transcriptome. IAT-resident ADIPOMAT were more abundant in higher BMI donors, while SAT-resident ADIPOMAT associated with impaired glycemia. TSHZ3 was identified as a candidate regulator of ADIPOMAT transcriptome. TSHZ3 knockdown in adipogenic progenitors inhibited differentiation, with downregulation of early adipogenic regulators (e.g. CEBPA/B, PPARG) and mature adipocyte genes. Heterozygous deletion of in mice reduced SAT and IAT weight. Here, we show that adipocyte subsets with distinct transcriptomic signature reside in human WAT; altered TSHZ3-mediated transcriptional regulation may contribute to low-maturation subpopulation linked to metabolic disease. - Source: PubMed
Publication date: 2025/09/16
Efthymiou VissarionGhosh AdhidebKodani Sean DCaubit XavierFasano LaurentAli WaqarPoulos Lindsay SCamara HenriqueGupta AnushkaBelaidouni YasmineBooeshaghi A SinaYang ShiyiRastogi RuchirShamsi FarnazVernon AshleyStreets AaronTseng Yu-HuaPatti Mary Elizabeth - Repetitive behaviors are cardinal features of many brain disorders, including autism spectrum disorder (ASD). We previously associated dysfunction of striatal cholinergic interneurons (SCINs) with repetitive behaviors in a mouse model based on conditional deletion of the ASD-related gene Tshz3 in cholinergic neurons (Chat-cKO). Here, we provide evidence linking SCIN abnormalities to the unique organization of the striatum into striosome and matrix compartments, whose imbalances are implicated in several pathological conditions. Chat-cKO mice exhibit an altered relationship between the embryonic birthdate of SCINs and their adult striosome-matrix distribution, leading to an increased proportion of striosomal SCINs. In addition, the ratio of striosomal SCINs with slow-irregular vs. sustained-regular firing is increased, which translates into decreased activity, further stressing the striosome-matrix imbalance. These findings provide novel insights into the pathogenesis of ASD-related stereotyped behaviors by pointing to abnormal developmental compartmentalization and activity of SCINs as a substrate. - Source: PubMed
Publication date: 2025/09/05
Molitor JordanGraniou JulietteSalin PascalCastets FrancisFatmi AhmedKerkerian-Le Goff LydiaFasano LaurentCaubit XavierGubellini Paolo