BAGE Forward PCR Primer (490bp position)
- Known as:
- BAGE Forward PCR test kit Primer (490bp position)
- Catalog number:
- MP1109
- Product Quantity:
- ea
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- BAGE Forward PCR Primer (490bp position)
Related genes to: BAGE Forward PCR Primer (490bp position)
- Gene:
- BAGE NIH gene
- Name:
- B melanoma antigen
- Previous symbol:
- -
- Synonyms:
- CT2.1, BAGE1
- Chromosome:
- 21p11.1 not on reference assembly
- Locus Type:
- gene with protein product
- Date approved:
- 1995-03-30
- Date modifiied:
- 2017-11-23
Related products to: BAGE Forward PCR Primer (490bp position)
Related articles to: BAGE Forward PCR Primer (490bp position)
- Breast cancer (BC) is the second most prevalent malignancy after lung cancer, and the life expectancy is still very low due to therapeutic resistance and tumor relapse. It is crucial to identify novel biomarkers that can serve as potential therapeutic targets. In TNBC, aberrant activation of EGFR has also been implicated in the development of drug resistance. STK35L1 is a critical regulator of diverse cellular processes, including apoptosis and DNA damage. Notably, STK35L1 promotes drug resistance and regulates glycolysis and apoptosis through AKT signaling. The oncogenic role of STK35L1 is established in various cancers, including osteosarcoma, colorectal cancer, and acute myeloid leukemia. However, its association in BC has not yet been explored. In this study, we found that STK35L1 was significantly upregulated in multiple cancers, and its higher expression was associated with poor survival outcomes in BC patients. STK35L1 was differentially upregulated across all BC subtypes. An association between EGFR and STK35L1 expression was observed in normal breast tissues but not in BC. Interestingly, compared with normal breast tissue, EGFR mRNA expression is downregulated in BC tissues, with the greatest downregulation in the luminal B subtype and the least in TNBC. Furthermore, EGFR inhibition with gefitinib increased STAT3 phosphorylation at Tyr-705, and STK35L1 and EGFR gene expression were significantly upregulated. These data suggest that EGFR-STAT3 signaling may regulate STK35L1 and EGFR expression. In conclusion, we report an association of STK35L1 and EGFR in BC, highlighting STK35L1 as a potential prognostic biomarker and therapeutic target. - Source: PubMed
Publication date: 2026/09/04
Bage SaloniYadav ArpanaGaur KritikaGahlot KritikaPurva MukulSaini MaheshDadarwal SunitaGehlot PragyaKumari SudhanshuBhutra ShyamSawant Devesh MadhukarBrünnert DanielaKasliwal NeenaGoyal Pankaj - The synthesis and characterization of organo-selenium compounds have attracted considerable interest for decades, driven by the search for efficient catalysts and bioinspired antioxidants; the investigation and exploitation of selenium─metal motifs in biological and medicinal chemistry represent a recent development and constitute the focus of this review. Selenoproteins are targets of metal ions like mercury and cadmium, whose toxicity is associated with the formation of stable selenium─metal bonds impairing protein function. On the other hand, selenium─metal bonding provides a strategy for tuning both chalcogen and metal reactivity, potentially enhancing the pharmacological performance of metallodrugs. Coordination to transition metals can modify redox potentials, bond polarization, and reactivity, thereby enabling multifunctional compounds combining metal-based pharmacophores with the redox activity of selenium. These systems may modulate reactive oxygen species, inhibit enzymes, and enhance selective cytotoxicity toward cancer cells. The formation of selenium─metal bonds in biological environment can also alter the function of metalloproteins, accounting for the toxicity of organoselenides. By combining experimental structural and reactivity properties with mechanistic insights from computational chemistry, we highlight the unifying concepts that govern selenium─metal bonding and to illustrate how these concepts can guide the rational design of new classes of selenium-based functional molecules. - Source: PubMed
Publication date: 2026/09/04
Filippi MatteoRubbi AlessandroNogara Pablo ARibaudo GiovanniLippolis VitoRocha João B TOrian Laura - The 2018 Nursing and Midwifery Council's 'Future Nurse' standards introduced increased genericism to UK nursing education, prompting criticism from specialist fields concerned about diluted field-specific knowledge. This article reports on a curriculum innovation at one UK university that addressed local implementation challenges through targeted module development to include an increased number of field-specific modules alongside core content. Among others, two new modules were introduced, one on mental health for adult nursing students, and one on children and young people's mental health for both mental health and children's nursing students. Qualitative feedback revealed initial student hesitation about mental health content among adult nursing students, which improved by module completion. The children's mental health module demonstrated better alignment with student expectations. Despite implementation challenges, including appropriate content depth and delivery timing, both modules showed evidence of success. This curriculum innovation demonstrates a practical response to balancing generic competencies with field-specific expertise requirements. - Source: PubMed
Publication date: 2026/09/03
Baldwin LaurenceMcLeod JudithBage RachelNicol FrancesDixon MayaKhan LyndsayAlcock-Towse HelenGordon Donna-MarieShiels Catherine - Cyanate-based compounds have received increasing attention due to their neuroprotective and antioxidant properties, which can be further enhanced by the incorporation of selenium, a key element in redox regulation. In this study, five selenocyanate derivatives (1-5), differing by alkyl or aryl groups, were synthesized and systematically evaluated using an integrated in silico, in vitro, and in vivo approach to explore their pharmacological and toxicological potential. Computational analyses included predictions of pharmacokinetic and toxicological parameters (ADME/T), as well as molecular docking studies targeting neurotransmitter-related enzymes, namely acetylcholinesterase (AChE) and monoamine oxidases (MAO-A and B). Antioxidant activity was evaluated using multiple complementary in vitro assays, including DPPH, ABTS, FRAP, GST-like, and SOD-like, as well as cerebral reactive species (RS). Cerebral AChE, MAO-A, and MAO-B activities were also measured in vitro. In vivo experiments involved evaluating acute oral toxicity in female Swiss mice. In silico results indicated favorable ADME/T profiles and affinity of selenocyanates for the target neurochemical enzymes. In vitro assays revealed antioxidant capacity for selenocyanates, particularly for compounds 1, 4, and 5. All compounds inhibited cerebral AChE and MAO isoforms in vitro, with particular emphasis on compounds 2 and 4 as AChE inhibitors. Therefore, compounds 2 and 4 were tested in vivo and showed no acute toxicity at an oral dose of 50 mg/kg; however, at 300 mg/kg, compound 2 showed signs of toxicity, whereas compound 4 remained non-lethal. Taken together, these results highlight organoselenocyanates, especially compound 4, as promising candidates for the development of antioxidant and neuroprotective agents. - Source: PubMed
Publication date: 2026/07/31
da Rocha Maria Eduarda RibeiroPizzi Bruna Rafaelada Costa PâmellaHall Tácia KatianePaim Mariana ParronCordeiro PâmellaMenezes VictorNascimento VanessaBrüning César AugustoBirmann Paloma TabordaBortolatto Cristiani Folharini - Organophosphate pesticides, such as chlorpyrifos (CPF), remain widely used in agriculture despite major toxicological concerns, particularly those associated with acetylcholinesterase (AChE) inhibition. In this study, we investigated the toxicological profile of six phosphorus selenide (R-PSe) compounds using an integrated in silico and in vitro approach, with CPF as a reference compound. In silico analyses using OSIRIS and pkCSM predicted a low toxicological risk for all R-PSe compounds. Molecular docking suggested that compounds 1-4 interact with the AChE active site, whereas compounds 5 and 6 showed weak binding affinity. Consistently, compounds 1-4 inhibited rat cerebral AChE activity in vitro, with IC values ranging from 0.06 to 1.60 μM, while compounds 5 and 6 were inactive under the tested conditions. The SAR analyses indicate that a SeP linkage, aromatic moieties, hydrogen-bond-accepting substituents, and a less bulky, more rigid carbon chain, are associated with AChE inhibitory activity. Increasing substrate concentration did not modify the inhibitory effect of compounds 1-4, indicating that their inhibition was not overcome by excess substrate. None of the compounds had pro-oxidant activity, a recognized critical secondary action mechanism of organophosphates. Overall, these findings identify phosphorus selenides 1-4 as potent mammalian AChE inhibitors and highlight that their potential biological application requires careful toxicological assessment. - Source: PubMed
Publication date: 2026/06/26
Caldeira FabíolaMarques Luiza SZborowski Vanessa AngonesiRecchi Ana Maria SRamirez Romelly Eugenia RojasBastianello Yago CSilva Nádia C CZeni GilsonNogara Pablo AndreiNogueira Cristina W