HYAL3 Antibody
- Known as:
- HYAL3 Antibody
- Catalog number:
- XW-8001
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- HYAL3 Antibody
Related genes to: HYAL3 Antibody
- Gene:
- HYAL3 NIH gene
- Name:
- hyaluronidase 3
- Previous symbol:
- -
- Synonyms:
- LUCA-3, LUCA14, Minna14
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-17
- Date modifiied:
- 2018-08-02
Related products to: HYAL3 Antibody
Related articles to: HYAL3 Antibody
- This study aimed to elucidate the molecular mechanisms driving the comorbidity of pulmonary arterial hypertension and cardiomyopathy (PAH-CMP), identify key pathogenic genes, and explore potential therapeutic agents targeting these genes. - Source: PubMed
Publication date: 2026/04/10
Hu JianchuanZhang WanqunZeng QiurongYang MinZhang LiliXu Yunhu - Finding the causative mutations for musculoskeletal system development and health status is of a higher priority for all sport horse breeders' associations. Of the regulating proteins involved in animal ossification, 15 gene polymorphisms were chosen to be identified as connected with the nine fetlock and 14 hock bone structures measurements of 198 horses. All measurements were taken using X-rays of the limbs, which were available at the beginning and end of the horse training. The analysis of variance (GLM, SAS program) was performed taking into account identified training and horse-connected characteristics, and gene polymorphism. The larger size of the bone structure was achieved in the fetlock for the heterozygotes of , , , , and . The heterozygotes were superior to homozygotes in the hock for the following genes: , , , and . The lower homozygote values were obtained for GG in in fetlock measurements, TT for in fetlock, TT for in fetlock, CC for in the hock, TT for in the hock, and TT for in the hock than their opposite homozygote and heterozygote variants. and are expressed in the same way for most of the bone structures in both joints. - Source: PubMed
Publication date: 2025/10/02
Lewczuk DorotaWypchło MariaHecold MateuszBuczkowska RomaKorwin-Kossakowska Agnieszka - Attention-deficit/hyperactivity disorder (ADHD) is a common neurodevelopmental disorder with high heritability. A total of 27 genome-wide significant loci for ADHD were previously identified through genome-wide association studies (GWASs), but the identification of risk genes that confer susceptibility to ADHD has remained largely unexplored. - Source: PubMed
Publication date: 2024/11/05
Deng Ming-GangZhou XiuxiuLi XiaoyanLiu Jiewei - Chemical protein synthesis by amide-forming ligation of two unprotected peptide segments offers an effective strategy for the preparation of protein derivatives that are not accessible through bioengineering approaches. Herein, an unprecedented chemical ligation between peptides with C-terminal 2-mercaptobenzaldehyde (thiol-salicylaldehyde, TSAL) esters and peptides bearing N-terminal cysteine/penicillamine is reported. Reactive peptide TSAL esters can be obtained from peptide hydrazides in an operationally simple and highly effective manner. This chemoselective peptide ligation enables the rapid production of N,S-benzylidene acetal intermediates, which can readily be converted into native amide bonds even at sterically hindered junctions. In addition, the current method can be applied compatibly in concert with other types of ligations and subsequent desulfurization chemistry, thereby facilitating convergent protein synthesis. The effectiveness of this new method is also showcased by the total synthesis of proteins ubiquitin and hyalomin-3 (Hyal-3), the efficient synthesis of protein ubiquitin-fold modifier 1 (UFM1) via a C-to-N sequential TSAL ester-induced ligation strategy, and the chemical synthesis of protein Mtb CM through a combined strategy of Ser/Thr ligation and TSAL ester-induced ligations. - Source: PubMed
Publication date: 2024/10/23
Li CuicuiMa WengeJin Kang - Attention-deficit/hyperactivity disorder (ADHD) is a chronic psychiatric disease that often affects a patient's whole life. Research has found that genetics plays an important role in the development of ADHD. However, there is still a lack of knowledge about the tissue-specific causal effects of biological processes beyond gene expression, such as alternative splicing (AS) and DNA methylation (DNAm), on ADHD. In this paper, a multi-omics study was conducted to investigate the causal effects of the transcription and the DNAm on ADHD, by integrating ADHD genome-wide association data with quantitative trait loci data of gene expression, AS, and DNAm across 14 different brain tissues. The causal effects were estimated using four different two-sample Mendelian randomization methods. Finally, we also prioritized the expression of 866 genes showing significant causal effects, including COMMD5, ENSG00000271904, HYAL3, etc., within at least one brain tissue. We prioritized 966 unique genes that have statistically significant causal AS events, within at least one of the 14 different brain tissues. These genes include PPP1R16A, GGT7, TREM2, etc. Furthermore, through mediation analysis, 106 regulatory pathways were inferred where DNAm influences ADHD through gene expression or AS processes. Our research findings provide guidance for future experimental studies on the molecular mechanisms of ADHD development, and also put forward valuable knowledge for the prevention, diagnosis, and treatment of ADHD. - Source: PubMed
Wang JingkaiZhu Qiu-WenMai Jia-HaoZhang ShunWang YuqingLiang JiatongZhou Ji-Yuan