Polyclonal Rabbit BAIAP2L1 Antibody
- Known as:
- Polyclonal Rabbit BAIAP2L1 Antibody
- Catalog number:
- KA0379
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit BAIAP2L1 Antibody
Related genes to: Polyclonal Rabbit BAIAP2L1 Antibody
- Gene:
- BAIAP2L1 NIH gene
- Name:
- BAI1 associated protein 2 like 1
- Previous symbol:
- -
- Synonyms:
- IRTKS
- Chromosome:
- 7q21.3-q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-09
- Date modifiied:
- 2018-02-13
Related products to: Polyclonal Rabbit BAIAP2L1 Antibody
Related articles to: Polyclonal Rabbit BAIAP2L1 Antibody
- Pheochromocytomas and paragangliomas (PPGLs) are rare neuroendocrine tumors primarily involving the adrenal medulla and its associated paraganglia, with heterogeneous clinical behavior and complex molecular drivers. This study aimed to characterize DNA methylation and gene expression patterns in PPGLs to understand the molecular differences between tumor subtypes and malignancy. We performed an integrative analysis of DNA methylation (Illumina EPIC 850K) and gene expression profiles (Affymetrix microarrays) in 24 PPGLs, comparing these with The Cancer Genome Atlas (TCGA) data, to delineate cluster- and malignancy-specific epigenetic patterns. Comparison between pseudohypoxic Cluster I and kinase-signaling Cluster II tumors revealed 13 differentially methylated CpG sites, with a specific CpG within showing hypermethylation in Cluster II accompanied by increased expression, suggesting context-dependent gene body methylation effects. Benign versus malignant comparisons identified 101 differentially methylated CpGs, including hypermethylated CpG in and hypomethylated CpG in in malignant tumors. Pathway enrichment of differentially methylated genes revealed alterations in Notch signaling, adherens junctions, cytoskeletal regulation, and intracellular transport. Gene expression analysis demonstrated partial overlap between clusters, with malignant tumors exhibiting distinct transcriptional profiles involving RNA processing, metabolism, and adhesion pathways. Correlation between methylation and expression was generally limited, emphasizing that methylation-dependent gene regulation is a locus-specific and context-dependent regulation. These findings illustrate a complex interplay between epigenetic modifications and transcriptional programs in PPGLs, enhancing our understanding of molecular heterogeneity and tumor classification, and identifying candidate biomarkers and therapeutic targets for malignant progression. - Source: PubMed
Publication date: 2026/01/20
Tabebi MounaŁysiak MałgorzataGimm OliverSöderkvist Peter - Allergic asthma is a disease driven by T helper 2 (Th2) cells, eosinophilia, airway hyperresponsiveness (AHR), and IgE-secreting B cells. Asthma is largely controlled by corticosteroids and β adrenergic receptor agonists that target and relax airway smooth muscle (ASM). Immunoglobulin M (IgM) isotype secreted by naïve B cells is important for class switching but may have other undefined functions. We investigated the role of IgM in a house dust mite (HDM)-induced Th2 allergic asthma model. We sensitised wild-type (WT) and IgM-deficient (IgM KO) mice with HDM and measured AHR, and Th2 responses. We performed RNA sequencing on the whole lung of WT and IgM KO mice sensitised to saline or HDM. We validated our AHR data on human ASM by deleting genes using CRISPR and measuring contraction by single-cell force cytometry. We found IgM to be essential in AHR but not Th2 airway inflammation or eosinophilia. RNA sequencing of lung tissue suggested that IgM regulated AHR through modulating brain-specific angiogenesis inhibitor 1-associated protein 2-like protein 1 () and other genes. Deletion of led to a differential reduction in human ASM contraction when stimulated with TNF-α and Acetylcholine, but not IL-13. These findings have implications for future treatment of asthma beyond current therapies. - Source: PubMed
Publication date: 2025/12/16
Hadebe SabeloSavulescu Anca FlaviaKhumalo JermaineJones KatelynMangali SandisiweMthembu NontobekoMusaigwa FungaiMaepa WelcomeNdlovu HlumaniNgomti AmkeleScibiorek MartynaOkendo JavanBrombacher Frank - Endometriosis is a hormone-dependent disease, in the pathophysiology of which sex hormones (androgens, estrogens, etc.) are involved. The level of bioactive androgens/estrogens (in the free state) in the organism largely depends on sex hormone-binding globulin (SHBG), which binds/transports a significant portion of the androgens/estrogens of the body and, due to this, changes the amount of these hormones in a free state (bioactive), which may be important in the development of endometriosis. The study was devoted to identifying the link between the genetic determinants (single nucleotide polymorphisms [SNPs]) of SHBG (according to predating genome-wide associative studies [GWAS]) and the risk of endometriosis in the Caucasian women of Russia. The study was accomplished on a total sample of 1368 women (395 endometriosis; 973 endometriosis free [controls]). Nine loci with an impact on SHBG level in predating GWAS have been examined. The search for associations of these loci with endometriosis was carried out: both their independent effects and interlocus interactions with an in silico interpretation of the functionality/pathways in which endometriosis-related loci and strongly linked SNPs were involved have been evaluated. Polymorphic locus rs440837 (A > G) correlated with endometriosis development (recessive genetic model): the SHBG-raising genotype GG rs440837 (A > G) serves as a risk factor for the disease formation; its presence in the genotype almost doubles the risk of endometriosis (OR = 1.91; 95%CI = 1.13-2.98; p = 0.024; power = 81.13%). The SHBG-impacts of 7 SNPs from 9 analyzed loci such as rs17496332 (A > G) , rs780093 (C > T) , rs10454142 (T > C) , rs3779195 (T > A) , rs440837 (A > G) , rs7910927 (G > T) , and rs8023580 (T > C) interacting with each other have been endometriosis-associated. Endometriosis-causal SNP rs440837 (A > G) and 5 proxy SNPs determine the DNA interaction in the region of 3 genes (, , ) with 22 transcription factors and, due to this, affect the processes of development of the endocrine system, gene transcription regulation, TGF-beta signaling pathway, regulation of cell proliferation/differentiation, etc. In conclusion, the results of this study showed the endometriosis risk effect of the SHBG-impact polymorphic variants. - Source: PubMed
Publication date: 2025/11/30
Ponomareva TatianaAltukhova OxanaChurnosova MariaAristova InnaReshetnikov EvgenyChurnosov MikhailPonomarenko Irina - The main goal of this study was to consider the role of obesity/overweight as a potential modifier of associations between gene single nucleotide polymorphisms (SNPs) affecting the sex hormone-binding globulin level (SHBG) and uterine myoma (UM). In the two women cohorts differentiated by body mass index (BMI) (BMI ≥ 25, n = 782 [379 UM/403 control] and BMI < 25, n = 760 [190 UM/570 control]), the association of genome-wide association studies (GWAS)-correlated SHBG-tied nine loci with UM was studied by method logistic regression with a subsequent in-depth evaluation of the functionality of UM-causal loci and their strongly linked variants. BMI-conditioned differences in the associations of SHBG-tied loci with UM were revealed: in the BMI < 25 group, a variant rs17496332 (A/G) was UM-correlated (OR = 0.70; = 0.024), and in the BMI ≥ 25 cohort, a SNP rs3779195 (T/A) was UM-associated (OR = 1.53; 0.019). Both the UM-causal loci and their proxy SNPs have pronounced probable functionality in the organism as a whole, as well as in the liver (the SHBG synthesis place), adipose tissue, uterus, etc., thereby influencing significant processes for UM biology such as regulation of the gene transcription, embryogenesis/development, cell proliferation/differentiation/apoptosis, metabolism, lipid exchange, etc. In conclusion, the results of our work demonstrated, for the first time, the essential role of obesity/overweight as a meaningful modifier of associations between SHBG-tied polymorphisms and UM. - Source: PubMed
Publication date: 2025/09/17
Ponomarenko MarinaReshetnikov EvgenyChurnosova MariaAristova InnaAbramova MariaNovakov VitalyChurnosov VladimirPolonikov AlexeyChurnosov MikhailPonomarenko Irina - In this study we searched for correlations between polymorphic variants that determine sex hormone-binding globulin concentration (SHBG) and uterine fibroids (UFs). The work was performed on a sample of 1542 women (569 with UFs and 973 without UFs [control]), from whom we obtained experimental data on the distribution of nine single-nucleotide polymorphisms (SNPs) affecting the SHBG (data confirmed in genome-wide association studies [GWASs]). When searching for associations with UFs, both the independent effects of SNPs and the effects of their SNP-SNP interactions (SNP-SNP) were taken into account during the "deep study" of the functionality of seven important UF loci and 115 strongly linked [r ≥ 0.80] variants (an in silico methodology was used). As the results show, two SHBG-related SNPs correlated with UF risk: rs3779195 [T/A] (OR = 0.38; 95%CI = 0.20-0.91; p = 0.023) and rs440837 [A/G] (OR = 1.93; 95%CI = 1.17-3.14; p = 0.010). At the same time, seven SHBG-related SNPs interacting with each other (four models of such SNP-SNP [p ≤ 0.01)] were found to influence UF risk. These SHBG-related SNPs, determining susceptibility to UF, showed strong functional relevance and were involved in pathways of gene transcription regulation, interactions with hormone ligand-binding receptors, the content control of SHBG, testosterone, liver enzymes, lipids, etc. This study's results demonstrate the effect of significant SHBG-related genetic determinants of UF risk. - Source: PubMed
Publication date: 2025/07/21
Ponomarenko MarinaReshetnikov EvgenyChurnosova MariaAristova InnaAbramova MariaNovakov VitalyChurnosov VladimirPolonikov AlexeyPlotnikov DenisChurnosov MikhailPonomarenko Irina