LW-1 antibody - middle region (ARP35905_P050)
- Known as:
- LW-1 (anti-) - middle region (ARP35905_P050)
- Catalog number:
- arp35905_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- LW-1 antibody - middle region (ARP35905_P050)
Ask about this productRelated genes to: LW-1 antibody - middle region (ARP35905_P050)
- Gene:
- EPPIN NIH gene
- Name:
- epididymal peptidase inhibitor
- Previous symbol:
- SPINLW1
- Synonyms:
- EPPIN1, EPPIN2, EPPIN3, dJ461P17.2, WAP7, WFDC7, CT71
- Chromosome:
- 20q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-31
- Date modifiied:
- 2014-11-19
- Gene:
- EPPIN-WFDC6 NIH gene
- Name:
- EPPIN-WFDC6 readthrough
- Previous symbol:
- SPINLW1-WFDC6
- Synonyms:
- -
- Chromosome:
- 20q13.12
- Locus Type:
- readthrough
- Date approved:
- 2011-02-21
- Date modifiied:
- 2014-11-19
- Gene:
- LYG1 NIH gene
- Name:
- lysozyme g1
- Previous symbol:
- -
- Synonyms:
- SALW1939
- Chromosome:
- 2q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2007-06-28
- Date modifiied:
- 2016-01-12
Related products to: LW-1 antibody - middle region (ARP35905_P050)
Related articles to: LW-1 antibody - middle region (ARP35905_P050)
- Increased levels of proinflammatory markers have been reported in tissues of individuals with Coronavirus Disease 2019 (COVID-19). We hypothesize that inflamed dental pulp tissues of individuals with previous history of COVID-19 may present a differential inflammatory gene expression profile in comparison with individuals who never had COVID-19. - Source: PubMed
Publication date: 2023/05/12
Cho Han NaChaves de Souza LeticiaJohnson CleverickKlein John RKirkpatrick Timothy CSilva RenatoLetra Ariadne - Cancer antigen-specific T cells are key components in antitumor immune response, yet their identification in the tumor microenvironment remains challenging, as most cancer antigens are unknown. Recent advance in immunology suggests that similar T-cell receptor (TCR) sequences can be clustered to infer shared antigen specificity. This study aims to identify antigen-specific TCRs from the tumor genomics sequencing data. - Source: PubMed
Publication date: 2019/12/12
Zhang HongyiLiu LongchaoZhang JianChen JiahuiYe JianfengShukla SachetQiao JianZhan XiaoweiChen HaoWu Catherine JFu Yang-XinLi Bo - Skin collagen Long Wavelength Fluorescence (LWF) is widely used as a surrogate marker for accumulation of advanced glycation end-products. Here we determined the relationship of LWF with glycemia, skin fluorescence, and the progression of complications during EDIC in 216 participants from the DCCT. - Source: PubMed
Publication date: 2016/02/11
Sell David RSun WanjieGao XiaoyuStrauch ChristopherLachin John MCleary Patricia AGenuth Saul Monnier Vincent M - Scleroderma (SSc) is a rare connective tissue disease characterized by fibrosis, microvasculopathy and autoimmune features. The role of genetics is limited in SSc, as suggested by similar concordance rates in monozygotic and dizygotic twin pairs, while environmental factors may act through epigenetic changes, as demonstrated for specific genes. Further, sex chromosome changes have been reported in SSc and may explain the female preponderance. In the present study we compared the methylation profile of all X chromosome genes in peripheral blood mononuclear cells from monozygotic twins discordant (n=7) and concordant (n=1) for SSc. Methylated DNA immunoprecipitations from each discordant twin pair were hybridized to a custom-designed array included 998 sites encompassing promoters of all X chromosome genes and randomly chosen autosomal genes. Biostatistical tools identified sites with an elevated probability to be consistently hypermethylated (n=18) or hypomethylated (n=25) in affected twins. Identified genes include transcription factors (ARX, HSFX1, ZBED1, ZNF41) and surface antigens (IL1RAPL2, PGRMC1), and pathway analysis suggests their involvement in cell proliferation (PGK1, SMS, UTP14A, SSR4), apoptosis (MTM1), inflammation (ARAF) and oxidative stress (ENOX2). In conclusion, we propose that X chromosome genes with different methylation profiles in monozygotic twin pairs may constitute candidates for SSc susceptibility. - Source: PubMed
Selmi CFeghali-Bostwick C ALleo ALombardi S ADe Santis MCavaciocchi FZammataro LMitchell M MLasalle J MMedsger TGershwin M E - Genomic rearrangements are a well-recognized cause of genetic disease and can be formed by a variety of mechanisms. We report a complex rearrangement causing severe hemophilia A, identified and further characterized using a range of PCR-based methods, and confirmed using array-comparative genomic hybridization (array-CGH). This rearrangement consists of a 15.5-kb deletion/16-bp insertion located 0.6 kb from a 28.1-kb deletion/263-kb insertion at Xq28 and is one of the most complex rearrangements described at a DNA sequence level. We propose that the rearrangement was generated by distinct but linked cellular responses to double strand breakage, namely break-induced replication (BIR) and a novel model of break-induced serial replication slippage (SRS). The copy number of several genes is affected by this rearrangement, with deletion of part of the Factor VIII gene (F8, causing hemophilia A) and the FUNDC2 gene, and duplication of the TMEM185A, HSFX1, MAGEA9, and MAGEA11 genes. As the patient exhibits no clinically detectable phenotype other than hemophilia A, it appears that the biological effects of the other genes involved are not dosage-dependent. This investigation has provided novel insights into processes of DNA repair including BIR and the first description of SRS during repair in a pathological context. - Source: PubMed
Sheen Campbell RJewell Ursula RMorris Christine MBrennan Stephen OFérec ClaudeGeorge Peter MSmith Mark PChen Jian-Min