PREB EMSA Probe Set
- Known as:
- PREB EMSA Probe Set
- Catalog number:
- AY1388P
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- PREB EMSA Probe Set
Related genes to: PREB EMSA Probe Set
- Gene:
- PREB NIH gene
- Name:
- prolactin regulatory element binding
- Previous symbol:
- -
- Synonyms:
- SEC12
- Chromosome:
- 2p23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-17
- Date modifiied:
- 2016-10-05
Related products to: PREB EMSA Probe Set
(+) Control probe (DNA), biotinylated(+) Control probe (RNA), biotinylated(-) Control probe (DNA), biotinylated(-) Control probe (RNA), biotinylated0.2 mm, 30 cm Spacer Set
0.2 mm, 30 cm Spacer Set0.35 mm, 30 cm Spacer Set
0.35 mm, 30 cm Spacer Set0.5 mm, 30 cm Spacer Set
0.5 mm, 30 cm Spacer Set0.75 mm Dual Gel Cast Set
0.75 mm Dual Gel Cast Set0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
Related articles to: PREB EMSA Probe Set
- GLP-1RAs improve glycemia and body weight, but their effects extend beyond insulin secretion and appetite suppression. Experimental evidence indicates that GLP-1 receptor signaling can relieve lipotoxic stress by reducing lipid influx, restoring lipid trafficking, promoting cholesterol efflux, improving mitochondrial and endoplasmic reticulum homeostasis, and suppressing inflammatory and apoptotic signaling. In pancreatic beta cells, saturated fatty acids, oxidized low-density lipoprotein and excess free cholesterol disrupt membrane microdomains, insulin-granule trafficking, calcium signaling, autophagic flux and beta-cell identity. Preclinical studies with individual GLP-1RAs, principally exendin-4 and liraglutide, implicate cAMP/PKA, PI3K/Akt, ERK1/2, AMPK, Nrf2 and autophagy-related pathways in these protective responses. A relevant mechanism is induction of ATP-binding cassette transporter A1 (ABCA1): exendin-4 stimulates ABCA1 transcription through the CaMKK/CaMKIV/PREB axis, linking incretin signaling to cholesterol export and preservation of glucose-stimulated insulin secretion. Recent work indicates spatially organized GLP-1R signaling at endoplasmic reticulum-mitochondria contact sites. Preclinical genetic evidence in mouse metabolic dysfunction-associated steatohepatitis (MASH) models indicates that pericentral liver sinusoidal endothelial GLP-1 receptors contribute to weight-loss-independent semaglutide-mediated improvements in steatosis, fibrosis and immune remodeling; whether an analogous causal mechanism operates in human MASH remains unknown. This review integrates systemic nutrient unloading, beta-cell cholesterol homeostasis and intrahepatic endothelial signaling as complementary mechanisms of metabolic protection. - Source: PubMed
Publication date: 2026/09/20
Jiang WenyiFukunaga KensakuKobayashi ToshihiroSaheki TakanobuYoshimura TakafumiZhang HaotianLy RathanaImachi HitomiMurao Koji - B-cell acute lymphoblastic leukemia (ALL) is a hematologic malignancy characterized by the abnormal proliferation of immature B-lineage lymphoblasts. Automated analysis of peripheral blood smear images may improve the speed and consistency of cell classification while supporting specialist interpretation. In this study, a cloud-based artificial intelligence image classification model was developed to differentiate benign hematogones from early pre-B, pre-B, and pro-B ALL categories. The model was trained and evaluated using 3,208 microscopic images from a publicly available dataset. Images were divided into training, validation, and testing subsets containing 2,568, 320, and 320 images, respectively, and model development was performed using Google Cloud AutoML (Google LLC, California, US). Performance was evaluated using average precision, precision, recall, precision-recall analysis, confidence-threshold evaluation, and a multiclass confusion matrix. At a confidence threshold of 0.50, the model achieved an average precision of 1.00, a precision of 100%, and recall of 99.4%. Class-specific correct classification rates were 100% for benign hematogones, early pre-B ALL, and pro-B ALL, and 98% for pre-B ALL, with the remaining pre-B images classified as early pre-B ALL. These findings demonstrate strong image-level performance within the internal testing dataset. External, multi-institutional, and patient-level validation is required before the model can be considered for clinical application. - Source: PubMed
Publication date: 2026/08/22
Bachir Mark ANawathey NeelBachir AlexReddy Akshay JGill SimranPatel Rakesh - Myeloid bias is a hallmark of aging and genotoxic stress, yet the mechanisms underlying the preferential suppression of lymphopoiesis and the resulting predominance of myeloid cells following DNA damage remain incompletely understood. Here, we systematically characterized the acute hematopoietic response to a clinically relevant 2 Gy dose of ionizing radiation in young adult mice. Forty-eight hours after irradiation, overall bone marrow cellularity was reduced by ~50-60%, with hematopoietic stem and progenitor cells (HSPCs) and myeloid populations declining proportionally. Strikingly, immature and naïve B cells in the bone marrow and developing T cells in the thymus exhibited profound hypersensitivity, declining by ~90%, thereby recapitulating the preferential vulnerability of lymphocytes to DNA damage. Single-cell RNA sequencing mapped this vulnerability to cells undergoing programmed clonal expansion associated with V(D)J recombination. Specifically, B and T lymphocytes immediately following productive V(D)J recombination at the immunoglobulin heavy-chain (IgH) and T-cell receptor β (TCRβ) loci were the most radiosensitive, resulting in the marked depletion of the immediately downstream small pre-B and CD4CD8 double-positive (DP) thymocyte populations. Mechanistically, this stage-specific radiosensitivity was mediated by ATM-dependent DNA damage responses, as deficiency selectively rescued the hypersensitivity of clonally expanding lymphoid progenitors while leaving the global reduction of HSPCs and myeloid cells largely unchanged. Rapidly proliferating S3 erythroblasts also exhibited a similar ATM-dependent hypersensitivity, suggesting that programmed proliferative bursts may represent a general determinant of radiation sensitivity. Together, these findings identify programmed clonal expansion associated with V(D)J recombination as an intrinsic developmental vulnerability that underlies the preferential suppression of lymphopoiesis following DNA damage and provides a mechanistic explanation for the emergence of myeloid bias. - Source: PubMed
Publication date: 2026/08/11
Lee Katherine HShao ZhengpingWang YunyueLee Brian JLi AngelinaYan FayeSims Peter AZha Shan - Acute respiratory distress syndrome (ARDS) is a complex clinical condition lacking reliable biomarkers that reflect underlying biological injury and predict clinical outcomes. Extracellular nicotinamide phosphoribosyltransferase (eNAMPT), an upstream inflammatory mediator implicated in endothelial injury, has emerged as a potential biomarker in ARDS. However, its association with ARDS onset and mortality has not been systematically synthesized. This review aimed to evaluate the association between circulating eNAMPT levels, ARDS onset, and mortality through a systematic review and meta-analysis. - Source: PubMed
Publication date: 2026/08/20
Srinivas ThejeshHanumaiah GaganaNagendra DanavathChaudhuri SouvikVasudeva AkhilaRao ShwethapriyaBhat Vinutha RPrakash Prabha - SWI/SNF chromatin remodeling complexes regulate gene expression during development and differentiation. These complexes exist in distinct forms, including the polybromo-associated BAF (PBAF) complex, defined by the ARID2 subunit. ARID2 is frequently mutated in B cell leukemias, but its role in normal B cell development remains unknown. Using Mb1-Cre and CD19-Cre conditional mouse models, we show that Arid2 is required for normal peripheral B-cell maturation. Early deletion with Mb1-Cre caused marked reductions in splenic T1 and T2 transitional B cells, follicular B cells, and recirculating B cells, whereas later deletion with CD19-Cre produced a milder follicular B cell phenotype but a similar reduction in transitional B cells. Bone-marrow progenitor and immature B cell populations were largely preserved, suggesting that the developmental defect emerges during peripheral transitional maturation and follicular B cell differentiation. Transcriptomic profiling of isolated pro-B, pre-B, and follicular B cells revealed that Arid2 loss caused progressive, stage-specific transcriptional dysregulation, including altered AP-1-associated programs and reduced B cell receptor-associated signaling in pre-B and follicular B cells. Functionally, mice with Mb1-Cre-mediated Arid2 deletion mice formed smaller germinal center B cell populations after immunization but maintained total and antigen-specific IgG responses and exhibited increased IgM responses. Together, these findings establish an important role for Arid2 in peripheral B cell maturation and germinal center responses. - Source: PubMed
Paolini Rachel LZimmerman Sarah MMarjai SadraSmith Sofia RChen Pei-YuSouroullas George P