Antxr2, 32-318aa, Mouse, His tag, Baculovirus
- Known as:
- Antxr2, 32-318aa, Mouse, detection labelled, Baculovirus
- Catalog number:
- atgp3325
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ATGen
- Gene target:
- Antxr2 32-318aa Mouse His tag Baculovirus
Related genes to: Antxr2, 32-318aa, Mouse, His tag, Baculovirus
- Gene:
- ANTXR2 NIH gene
- Name:
- ANTXR cell adhesion molecule 2
- Previous symbol:
- -
- Synonyms:
- CMG2, CMG-2, FLJ31074
- Chromosome:
- 4q21.21
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-25
- Date modifiied:
- 2018-05-10
Related products to: Antxr2, 32-318aa, Mouse, His tag, Baculovirus
Related articles to: Antxr2, 32-318aa, Mouse, His tag, Baculovirus
- is the bacterium responsible for causing the zoonotic disease called anthrax. The disease presents itself in different forms like gastrointestinal, inhalation, and cutaneous. Bacterial spores are tremendously adaptable, can persist for extended periods and occasionally endanger human health. The Anthrax Toxin Receptor-2 () gene acts as membrane receptor and facilitates the entry of the anthrax toxin into host cells. Additionally, mutations in the gene have been linked to various autoimmune diseases, including Hyaline Fibromatosis Syndrome (HFS), Ankylosing Spondylitis (AS), Juvenile Hyaline Fibromatosis (JHF), and Infantile Systemic Hyalinosis (ISH). This study delves into the genetic landscape of , aiming to comprehend its associations with diverse disorders, elucidate the impacts of its mutations, and pinpoint minimal non-pathogenic mutations capable of reducing the binding affinity of the gene with the protective antigen. Recognizing the pivotal role of single-nucleotide polymorphisms (SNPs) in shaping genetic diversity, we conducted computational analyses to discern highly deleterious and tolerated non-synonymous SNPs (nsSNPs) in the gene. The Mutpred2 server determined that the Arg465Trp alteration in the gene leads to altered DNA binding ( = 0.22) with a probability of a deleterious mutation of 0.808; notably, among the identified deleterious SNPs, rs368288611 (Arg465Trp) stands out due to its significant impact on altering the DNA-binding ability of . We propose these SNPs as potential candidates for hypertension linked to the gene, which is implicated in blood pressure regulation. Noteworthy among the tolerated substitutions is rs200536829 (Ala33Ser), recognized as less pathogenic; this highlights its potential as a valuable biomarker, potentially reducing side effects on the host while also reducing binding with the protective antigen protein. Investigating these SNPs holds the potential to correlate with several autoimmune disorders and mitigate the impact of anthrax disease in humans. - Source: PubMed
Publication date: 2024/03/28
Archana Chamalapura AshwathamaSekar Yamini SriSuresh Kuralayanapalya PuttahonnappaSubramaniam SaravananSagar NingegowdaRani SwatiAnandakumar JayashreePandey Rajan KumarBarman Nagendra NathPatil Sharanagouda S - Stroke is a disease with high morbidity, disability, and mortality. Immune factors play a crucial role in the occurrence of ischemic stroke (IS), but their exact mechanism is not clear. This study aims to identify possible immunological mechanisms by recognizing immune-related biomarkers and evaluating the infiltration pattern of immune cells. - Source: PubMed
Publication date: 2024/04/19
Cong LinHe YijieWu YunLi ZeDing SiwenLiang WeiweiXiao XingjunZhang HuixueWang Lihua - Hyaline fibromatosis syndrome is an extremely rare autosomal recessive condition caused by biallelic pathogenic variants in the ANTXR2 gene that leads to abnormal growth of hyalinized fibrous tissue. Severity ranges from life-threatening intractable diarrhea, recurrent infection, and acute pain to milder disease resulting in skin lesions and less severe contractures. Here, we report the case of a 3-month-old female who presented with joint contractures and severe pain followed by failure to thrive. Diagnosis via ultra-rapid whole genome sequencing allowed our team to provide appropriate care and anticipatory guidance for this patient and family. - Source: PubMed
Publication date: 2024/02/21
Anderson Sharon - Hepatocellular carcinoma is one of the leading cancers worldwide and is a potential consequence of fibrosis. Therefore, the identification of key cellular and molecular mechanisms involved in liver fibrosis is an important goal for the development of new strategies to control liver-related diseases. Here, single-cell RNA sequencing data (GSE136103 and GES181483) of clinical liver non-parenchymal cells were analyzed to identify cellular and molecular mechanisms of liver fibrosis. The proportion of endothelial subpopulations in cirrhotic livers was significantly higher than that in healthy livers. Gene ontology and gene set enrichment analysis of differentially expressed genes in the endothelial subgroups revealed that extracellular matrix (ECM)-related pathways were significantly enriched. Since anthrax toxin receptor 2 (ANTXR2) interacts with the ECM, the expression of ANTXR2 in the liver endothelium was analyzed. ANTXR2 expression in the liver endothelium of wild-type (WT) mice significantly decreased after a 4-time sequential injection of carbon tetrachloride (CCl) to induce liver fibrosis. Next, conditional knockout mice selectively lacking in endothelial cells were generated. After endothelial-specific knockout mice were subjected to the CCl model, the degree of liver fibrosis in the knockout group was significantly more severe than that in the control group. In addition, ANTXR2 in human umbilical vein endothelial cells promoted matrix metalloproteinase 2 (MMP2) activation to degrade the ECM . Finally, endothelial-specific overexpression of alleviated the development of liver fibrosis following adeno-associated virus treatment. Collectively, these results suggested that endothelial ANTXR2 plays a protective role in liver fibrosis. This function of ANTXR2 may be achieved by promoting MMP2 activation to degrade the ECM. - Source: PubMed
Publication date: 2024/01/23
Huang XiaojuanZhang LiyinLuo WeiZeng YuLi XiaoxueYang NanHuang WenwenDing Bi-Sen - Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease affecting over 30,000 people in the United States. It is characterized by the progressive decline of the nervous system that leads to the weakening of muscles which impacts physical function. Approximately, 15% of individuals diagnosed with ALS have a known genetic variant that contributes to their disease. As therapies that slow or prevent symptoms, such as antisense oligonucleotides, continue to develop, it is important to discover novel genes that could be targets for treatment. Additionally, as cohorts continue to grow, performing analyses in ALS subtypes, such as primary lateral sclerosis (PLS), becomes possible due to an increase in power. These analyses could highlight novel pathways in disease manifestation. - Source: PubMed
Publication date: 2023/12/21
Pottinger Tess DMotelow Joshua EPovysil GundulaMoreno Cristiane A MartinsRen ZhongPhatnani Hemali Aitman Timothy JSantoyo-Lopez Javier Mitsumoto Hiroshi Goldstein David BHarms Matthew B