PREB EMSA Kit
- Known as:
- PREB EMSA Kit
- Catalog number:
- AY1388
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- PREB EMSA Kit
Related genes to: PREB EMSA Kit
- 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
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- Steatotic liver disease is a common metabolic disorder, and interleukin-1β (IL-1β) contributes to hepatic inflammation and lipid accumulation. ATP-binding cassette subfamily A member 1 (ABCA1) regulates cholesterol efflux and lipid homeostasis. This study examined whether IL-1β suppresses hepatic ABCA1 expression and explored the underlying signaling and transcriptional mechanisms. Primary mouse hepatocytes and HepG2 cells were treated with IL-1β. ABCA1 expression was assessed by Western blotting and RT-qPCR, and ABCA1 promoter activity was examined using luciferase reporter assays with inhibitors targeting phosphoinositide 3-kinase (PI3K), p38 mitogen-activated protein kinase (p38 MAPK), or an H-89-sensitive pathway. Prolactin regulatory element-binding protein (PREB) involvement was evaluated by nuclear protein analysis, PREB-binding-site mutation, and siRNA-mediated knockdown. Lipid accumulation was assessed by intracellular cholesterol measurement and Oil Red O staining. IL-1β decreased ABCA1 protein and mRNA expression in a dose- and time-dependent manner and suppressed ABCA1 promoter activity. Inhibition of p38 MAPK or treatment with H-89 attenuated IL-1β-induced suppression of promoter activity and endogenous ABCA1 expression. Representative immunoblotting showed that IL-1β enhanced p38 MAPK phosphorylation, whereas SB203580 attenuated this response. IL-1β reduced nuclear PREB expression, and p38 MAPK inhibition restored nuclear PREB expression. Mutation of the PREB-binding site or PREB knockdown abolished IL-1β-mediated suppression of ABCA1 expression. IL-1β also increased intracellular cholesterol content and Oil Red O-positive lipid accumulation. These findings suggest that IL-1β suppresses hepatic ABCA1 expression through p38 MAPK signaling and an H-89-sensitive pathway, at least partly involving PREB-associated transcriptional regulation, and that this suppression is associated with hepatocellular lipid accumulation. - Source: PubMed
Publication date: 2026/08/25
Lyu JingyaFukunaga KensakuHe ZhangchiImachi HitomiKobayashi ToshihiroSaheki TakanobuYoshimura TakafumiHarada EriIzumi KosukeJiang WenyiZhang HaotianRathana LyIwama HisakazuGuo JinghuiMurao Koji - Although cytarabine remains a cornerstone chemotherapeutic agent for Acute lymphoblastic leukemia (ALL), its clinical efficacy is frequently compromised by systemic toxicity and resistance mechanisms, notably telomerase activation via hTERT upregulation. This study investigates the synergistic potential of Zataria multiflora extract (ZME) combined with cytarabine to induce apoptosis in pre-B ALL cells (NALM-6) and explores the underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/08/14
Pilehvari NiloofarFatemi AhmadLashkari MahlaValandani Hajar MardaniAshoub Muhammad HosseinKhalilabadi Roohollah Mirzaee - B-cell precursor acute lymphoblastic leukemia (preB-ALL) is characterized by pathogenic variants currently used in precision oncology. However, the mutational landscape of Mexican children with preB-ALL has not yet been thoroughly explored and defined in terms of the clinical significance. We used a custom-designed next-generation sequencing exome panel, along with high-resolution chromosome microarrays and gene fusion-targeted assays, to characterize the mutational landscape of 73 Mexican children with preB-ALL, exploring the profile of clinically significant variants. We classified the variants following the AMP-ASCO-CAP 2017 and ACMG-CG 2019 guidelines recommendations. The mutational landscape includes a broad molecular spectrum of variants affecting cell cycle regulation, B-cell development, kinase signaling, and epigenetic regulation genes. Tier 1 diagnostic variants allowed the identification of pre-B ALL genetic subtypes, diminishing the preB-ALL NOS group from 63% to 37%. Furthermore, 37% of cases presented Tier 1 variants conferring intermediate to adverse prognoses (primarily involving CRLF2 gene fusions, as well as PAX5, IKZF1, and TP53 inactivating mutations). Notably, these patients exhibited high-risk clinical features and a lower event free survival rate than patients without these variants (60% versus 41.2%; p = 0.046; 95% CI). Between 19% and 42% of patients had Tier 2 variants targetable with JAK-STAT or RAS-MAPK signaling inhibitors. These patients showed a lower overall survival rate than patients without these variants (64% versus 90%; p = 0.048; 95% CI). Tier 1 potential germline variants in cancer predisposition genes (mainly BRCA1/2 and CHEK2) were observed in 10% of patients, some of whom had a family history of cancer. This highlights the importance of genetic counseling for patients and their families. Finally, 33% of patients had Tier 3 variants that were predicted to be deleterious and potentially upgraded to pathogenic with plausible clinical relevance. In conclusion, the mutational landscape analysis revealed variants useful for oncologic management and genetic counseling of Mexican children with preB-ALL. - Source: PubMed
Martínez Anaya DanielJuárez-Velázquez María Del RocíoJuárez Figueroa UlisesDean MichaelSalas Labadía ConsueloValladares Coyotecatl MarianReyes León AdrianaLópez Santiago NormaJuárez Villegas LuisZapata Tarrés MartaPérez-Vera Patricia - Natural Killer Lytic-Associated Molecule (NKLAM) (also known as RNF19b) is a membrane-bound E3 ubiquitin ligase. Previous studies demonstrated a role of NKLAM in natural killer (NK) cell function and pro-inflammatory cytokine production by macrophages. Studies using lymphoma, melanoma and breast cancer cells found that tumor dissemination and metastasis are greater in NKLAM-deficient knockout (KO) mice than in wild type (WT) mice, indicating that NKLAM participates in controlling tumor development . - Source: PubMed
Publication date: 2026/07/15
Hoover Richard GMatchett Emily CKornbluth Jacki - Acute lymphoblastic leukemia (ALL) is the most common pediatric malignancy and is associated with profound metabolic reprogramming. This exploratory study aimed to characterize the metabolomic profiles of plasma and cerebrospinal fluid (CSF) in children with newly diagnosed pre-B-cell acute lymphoblastic leukemia (pre-B ALL) prior to therapy. Metabolomic analyses were performed using mass spectrometry-based platforms combined with multivariate statistical approaches (PCA, OPLS-DA, SVM-RFE, EBAM). In plasma, we identified 41 significantly altered metabolites (FDR < 0.011), revealing a distinct signature that differentiated pre-B ALL patients from healthy controls. Specifically, patients exhibited elevated levels of hypoxanthine, xanthine, and phosphatidylcholine derivatives, alongside reduced concentrations of -cysteine and prasterone sulfate, indicating systemic dysregulation of purine, lipid, and amino acid metabolism. In CSF, we observed a distinct metabolic profile characterized by coordinated disturbances in purine degradation, phospholipid metabolism, and sphingolipid pathways. Notably, correlation analysis between the two matrices suggested that systemic metabolic shifts, particularly in purine metabolism (e.g., hypoxanthine and xanthine levels), are mirrored within the central nervous system microenvironment. These findings indicate that children with pre-B ALL exhibit specific metabolic alterations in both compartments before treatment. This work serves as a proof-of-concept for applying metabolomics in pediatric oncology, highlighting the necessity for further validation in larger, prospective cohorts to assess the clinical utility of these profiles. - Source: PubMed
Publication date: 2026/07/12
Wasilewski AndrzejCzapor-Irzabek HannaŚciskalska MilenaEl Idrissi AdamChegdani FatimaMatera-Witkiewicz AgnieszkaZatoński TomaszPołtyn-Zaradna KatarzynaBrutkowski TomaszKlimczak AleksandraKazanowska BernardaSerrafi Agata