BETA_2 MICROGLOBULIN, Antibody (B2M)
- Known as:
- BETA_2 MICROGLOBULIN, Antibody (ß2-microglobulin)
- Catalog number:
- 126-113B12
- Product Quantity:
- 100 ug
- Category:
- Antibodies
- Supplier:
- LeeBio
- Gene target:
- BETA_2 MICROGLOBULIN Antibody (B2M)
Related genes to: BETA_2 MICROGLOBULIN, Antibody (B2M)
- Gene:
- B2M NIH gene
- Name:
- beta-2-microglobulin
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 15q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
- Gene:
- NEUROD1 NIH gene
- Name:
- neuronal differentiation 1
- Previous symbol:
- NEUROD
- Synonyms:
- BETA2, BHF-1, NeuroD, bHLHa3, MODY6
- Chromosome:
- 2q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-03-12
- Date modifiied:
- 2019-04-23
- Gene:
- PCDHB2 NIH gene
- Name:
- protocadherin beta 2
- Previous symbol:
- -
- Synonyms:
- PCDH-BETA2
- Chromosome:
- 5q31.3
- Locus Type:
- protocadherin
- Date approved:
- 2000-06-28
- Date modifiied:
- 2016-10-05
Related products to: BETA_2 MICROGLOBULIN, Antibody (B2M)
Related articles to: BETA_2 MICROGLOBULIN, Antibody (B2M)
- Emerging infectious diseases are one of the foremost contemporary threats to biodiversity conservation. Outbreaks of novel pathogens can lead to the extinction of host populations, loss of gene flow due to extirpation, and bottlenecks in host populations with surviving individuals. In outbreaks with survivors, pathogens can exert strong selection on hosts, in some cases leading to the evolution of resistance or tolerance in the host population. The pathogen causing sylvatic plague, , was introduced to North America in the early 1900s and caused widespread population declines in prairie dogs (genus ), which experience >95% mortality during epizootics. Recently, survival from plague was documented in a small number of black-tailed prairie dogs () in natural populations in Colorado (United States). We performed whole-genome sequencing on all seven individuals that survived infection with plague and seven individuals that likely died. Using genome-wide association tests, outlier tests, and other inferences of selection, we detected single nucleotide polymorphisms (SNPs) on five scaffolds that were strongly associated with survivorship from plague in nature. One candidate gene, inducible T-cell stimulator (), was also associated with survival in humans during the Black Death in London (United Kingdom), suggesting conservation of gene function across taxonomically diverse lineages. In addition, three candidate genes (, , and ) are different from but in the same gene classes (transmembrane proteins, protocadherins, and Kasuza protein-binding genes) as candidate genes for plague resistance in great gerbils, providing support for the hypothesis that parallel evolution may occur at the level of gene classes in addition to individual genes. Understanding the genomic basis of immunity can enable genetically informed management actions, such as targeted relocation to protect grassland species. Moreover, understanding how rapid adaptation to pathogens occurs can help us predict the time frame and spatial scale at which adaptation may occur, during which other interventions are needed. - Source: PubMed
Publication date: 2025/07/08
Cassin-Sackett LorenTsuchiya Mirian T NDikow Rebecca B - Asthma is a genetically complex inflammatory airway disease associated with more than 200 SNPs. However, the functional effects of many asthma-associated SNPs in lung and airway epithelial samples are unknown. Here, we aimed to conduct expression quantitative trait loci (eQTL) analysis using a meta-analysis of nasal and lung samples. We hypothesize that incorporating cell type proportions of airway and lung samples enhances eQTL analysis outcomes. Nasal brush ( = 792) and lung tissue ( = 1,087) samples were investigated separately. Initially, a general eQTL analysis identified genetic variants associated with gene expression levels. Estimated cell type proportions were adjusted based on the Human Lung Cell Atlas. In addition, the presence of significant interaction effects between asthma-associated SNPs and each cell type proportion was explored and considered evidence for cell type-associated eQTL. In nasal brush and lung parenchyma samples, 44 and 116 asthma-associated SNPs were identified as eQTL. Adjusting for cell type proportions revealed eQTL for an additional 17 genes (e.g., , , and ) and 16 genes (e.g., , , and ) in nose and lung, respectively. Moreover, we identified eQTL for nine SNPs annotated to genes such as , , and displayed significant interactions with cell type proportions of club, goblet, and alveolar macrophages. Our findings demonstrate increased power for identifying eQTL among asthma-associated SNPs by considering cell type proportion of the bulk RNA-sequencing data from nasal and lung tissues. Integration of cell type deconvolution and eQTL analysis enhances our understanding of asthma genetics and cellular mechanisms, uncovering potential therapeutic targets for personalized interventions. - Source: PubMed
El-Husseini Zaid WKarp TatianaLan AndyGillett Tessa EQi CancanKhalenkow Dmitryvan der Molen ThysBrightling ChrisPapi AlbertoRabe Klaus FSiddiqui SalmanSingh DaveKraft MonicaBeghé BiancaJoubert PhilippeBossé YohanSin DonCordero Ana HTimens WimBrandsma Corry-AnkeHao KeNickle David CVonk Judith MNawijn Martijn Cvan den Berge MaartenGosens ReinoudFaiz AlenKoppelman Gerard H - Emerging evidence has proven that ferroptosis plays an important role in the development of acute myeloid leukemia (AML), whereas the exact role of ferroptosis-associated genes in AML patients' prognosis remained unclear. Gene expression profiles and corresponding clinical information of AML cases were obtained from the TCGA (TCGA-LAML), GEO (GSE71014), and TARGET databases (TARGET-AML). Patients in the TCGA cohort were well-grouped into two clusters based on ferroptosis-related genes, and differentially expressed genes were screened between the two clusters. Univariate Cox and LASSO regression analyses were applied to select prognosis-related genes for the construction of a prognostic risk-scoring model. Survival analysis was analyzed by Kaplan-Meier and receiver operator characteristic curves. Furthermore, we explored the correlation of the prognostic risk-scoring model with immune infiltration and chemotherapy response. Risk gene expression level was detected by quantitative reverse transcription polymerase chain reaction. Eighteen signature genes, including ZSCAN4, ASTN1, CCL23, DLL3, EFNB3, FAM155B, FOXL1, HMX2, HRASLS, LGALS1, LHX6, MXRA5, PCDHB12, PRINS, TMEM56, TWIST1, ZFPM2, and ZNF560, were developed to construct a prognostic risk-scoring model. AML patients could be grouped into high- and low-risk groups, and low-risk patients showed better survival than high-risk patients. Area under the curve values of 1, 3, and 5 years were 0.81, 0.827, and 0.786 in the training set, respectively, indicating a good predictive efficacy. In addition, age and risk score were the independent prognostic factors after univariate and multivariate Cox regression analyses. A nomogram containing clinical factors and prognostic risk-scoring model was constructed to better estimate individual survival. Further analyses demonstrated that risk score was associated with the immune infiltration and response to chemotherapy. Our experiment data revealed that LGALS1 and TMEM56 showed notably decreased expression in AML samples than that of the normal samples. Our study shows that the prognostic risk-scoring model and key risk gene may provide potential prognostic biomarkers and therapeutic option for AML patients. - Source: PubMed
Publication date: 2022/01/21
Wang JinghuaZhuo ZeweiWang YanjunYang ShuoChen JierongWang YulianGeng SuxiaLi MinmingDu XinLai PeilongWeng Jianyu - To study the diversity of the protocadherin family, the cDNA clones for a novel protocadherin were isolated by screening rat brain cDNA libraries with a cDNA fragment obtained by PCR, and some of the properties were then characterized. The overall structure of the protein defined by the clone is similar to that of previously identified protocadherins; however, the cytoplasmic domain is distinct from those of previously cloned protocadherins or any other protein sequences in the data bank. We named this protocad herin-3 (Pcdh3) since this is the third protocadherin of which the entire coding sequence has been determined. Most of the deduced amino acid sequences of other cDNA clones obtained by the screening show high homology with but are distinct from that of Pcdh3, indicating that most of these sequences correspond to homologous but different protocadherins. These results demonstrate that Pcdh3 and the protocadherins defined by these clones constitute a protocadherin subfamily. Chromosome mapping indicates that mouse Pcdh3 is located in a specific region of mouse chromosome 18, close to the location of previously cloned protocadherins, suggesting that various protocadherins form a cluster in this region. In situ hybridization results showed that Pcdh3 and its related proteins were expressed at various areas in brain. The expressed Pcdh3 protein from the cDNA in mouse L cells was about 100 kDa in molecular weight and was localized at cell-cell contact sites. In contrast to the classical cadherins, however, the expressed Pcdh3 was sensitive to trypsin even in the presence of Ca2+, and the transfectants did not show strong Ca(2+)-dependent cell aggregation activity. These results indicate the structural and possibly functional diversity of the protocadherin family and suggest a distinctive biological role for Pcdh3. - Source: PubMed
Sago HKitagawa MObata SMori NTaketani SRochelle J MSeldin M FDavidson MSt John TSuzuki S T