PGLS 293T Cell Transient Overexpression Lysate(Denatured)
- Known as:
- PGLS 293T Cell Transient Overexpression Lysate(Denatured)
- Catalog number:
- H00025796-T01
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- PGLS 293T Cell Transient Overexpression Lysate(Denatured)
Related genes to: PGLS 293T Cell Transient Overexpression Lysate(Denatured)
- Gene:
- PGLS NIH gene
- Name:
- 6-phosphogluconolactonase
- Previous symbol:
- -
- Synonyms:
- 6PGL
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-20
- Date modifiied:
- 2015-08-25
Related products to: PGLS 293T Cell Transient Overexpression Lysate(Denatured)
Related articles to: PGLS 293T Cell Transient Overexpression Lysate(Denatured)
- Paragangliomas (PGLs) are uncommon neuroendocrine tumors of extra-adrenal origin, and involvement of the vulva is exceptionally rare, often creating diagnostic difficulty due to morphological overlap with other neoplasms. We report a case of 35-year-old female with a prior history of pheochromocytoma who presented with a vulvar mass. Histopathological examination showed a tumor composed of nests and trabeculae (Zellballen pattern) of cells with neuroendocrine features, closely simulating other nested tumors. Immunohistochemical (IHC) analysis revealed strong synaptophysin, chromogranin, and CD56 expression, while the tumor cells were negative for cytokeratin, Melan-A, and S100, thereby excluding epithelial, melanocytic, and sustentacular lineages. A key finding was the loss of Succinate dehydrogenase subunit B (SDHB) expression along with a markedly elevated Ki-67 index (~60%), indicating aggressive biological behavior and raising the possibility of an underlying hereditary syndrome, for which genetic counseling is recommended. Integrating the histopathological findings with clinical and radiological data led to a diagnosis of Metastatic PGL. This case emphasizes the importance of a comprehensive IHC approach in accurately classifying such rare and clinically significant tumors. - Source: PubMed
Publication date: 2026/08/25
Kshirsagar Sayali PrakashRatnakar AshwiniGosavi Manasi A - The diversity of brain size and organization across mammals reflects how evolutionary and ecological pressures have shaped neural architecture through time. Yet, how these selective pressures translated into measurable variation in the proportions and overall shape of the brain across species remains poorly understood. In this study, we used high-resolution virtual endocasts from 41 musteloid species (e.g., otters, skunks, raccoons) to quantify variation in endocranial composition and shape. We analyzed both the complete endocast and its principal subdivisions (olfactory bulbs (OB), cerebrum, and hindbrain) using a combination of compositional data analysis and 3D geometric morphometrics. Phylogenetically informed regressions (PGLS) and model comparisons were used to assess the effects of endocranial size, locomotion, diet, and taxonomy on both the regional proportions and the overall shape of the endocranial cast. Musteloid brain organization is mostly driven by size-dependent scaling: larger brains have enlarged cerebra, reduced olfactory and hindbrain regions, and rounder endocasts. However, some lineages markedly deviate from this largely conserved allometry: otters (Lutrinae) exhibit proportionally enlarged cerebra and strongly reduced OB, whereas skunks (Mephitidae) show the reverse pattern, emphasizing enhanced olfactory investment. Feeding ecology also contributes to variation in brain organization, as piscivores show disproportionately smaller OB compared with other feeding guilds. In contrast, locomotor mode has little explanatory power for either endocranial composition or shape. Brain evolution in musteloids is therefore not uniform: a common scaling pattern dominates, but lineage- and diet-specific adjustments modify how brain regions are proportioned. - Source: PubMed
Publication date: 2026/08/23
Michaud MargotHarrington Arianna RoseLadeveze SandrineGálvez-López EloyFischer ValentinAlfsen ApollineBertrand Ornella - Paragangliomas (PGLs) are rare neural crest-derived tumors with highly variable morphology and clinical behavior. These tumors can present with cystic and necrotic alterations that may influence the clinical presentation of affected patients. However, prevalence and clinical significance of these pathological alterations remain poorly understood. In this retrospective study (2011-2021), 103 patients with confirmed PGLs were examined for cystic and necrotic alterations based on imaging and pathology reports as well as pathological re-evaluation. Cystic alterations, including microscopic, macroscopic, and pseudocystic alterations, were observed in 61.8% of PGLs. Regardless of their pathomorphological presentation, cystic alterations did not affect the clinical presentation of these patients. In contrast, necrotic alterations were identified in 3.9% of PGLs and were associated with a higher rate of metastasis (75% vs. 10%, p = 0.0124), larger tumor volume (53.6 cm vs. 6.6 cmp = 0.0339), and more pronounced signs and symptoms, including hypertension, palpitations, and weakness compared to patients without cystic/necrotic lesions. The prevalence of cystic and necrotic lesions was higher in adrenal than extra-adrenal PGLs. An additional meta-analysis of 235 patients with PGLs confirmed the increased rate of metastasis in necrotic PGLs (16% vs. 4.5%, p = 0.0369), which were also significantly more frequently associated with cardiovascular complications (p < 0.0001) than cystic PGLs. Considering pathological alterations, particularly necrotic lesions, may substantially affect the clinical management of patients with PGLs. Incorporating these features into preoperative management and follow-up strategies might be crucial, given the higher metastatic potential and increased cardiovascular risk associated with necrotic PGLs. - Source: PubMed
Publication date: 2026/08/22
Wiejak Anna-MariaConstantinescu GeorgianaZygiene GintareRobledo MercedesZiegler Christian GKühn Jens-Peterde Krijger RonaldPamporaki ChristinaMeinhardt MatthiasBechmann Nicole - Tuberculosis (TB), caused by Mycobacterium tuberculosis (M. tb), remains a major global health challenge and a leading cause of infectious mortality. Central to TB pathogenesis is the nuclear factor-kappa B (NF-κB) signaling network, a master regulator of inflammation, immune activation, and host defense. This review highlights the complex molecular interplay between M. tb virulence determinants and host NF-κB pathways, emphasizing how the pathogen strategically manipulates transcriptional responses to promote survival, persistence, and transmission. Early during infection, cell wall-derived muramyl dipeptide (MDP) activates the NOD2-RIP2 signaling axis, triggering canonical NF-κB activation and p50/RelA-dependent transcription of pro-inflammatory mediators essential for innate immune containment. However, persistent infection is characterized by extensive immune reprogramming. Antigen 85-derived trehalose dimycolate (TDM), biofilm-associated structures, phenolic glycolipids (PGLs), sulfatides, and the catalase-peroxidase enzyme KatG selectively suppress protective NF-κB responses through mechanisms involving p50/p50 homodimer accumulation, RelA repression, disruption of TLR2-MyD88 signaling, and inhibition of redox-dependent IKK activation. In parallel, the ESX-1-secreted ESAT-6/CFP-10 complex and stress-induced heat shock proteins drive persistent NF-κB hyperactivation, resulting in excessive cytokine production, matrix metalloproteinase release, tissue destruction, and bacterial dissemination. Furthermore, antigenic variation mediated by PE/PPE protein families continuously rewires receptor-dependent signaling pathways, preventing effective adaptive immune memory formation. Collectively, these findings reveal that M. tb does not merely evade host immunity but actively remodels NF-κB signaling dynamics through coordinated activation, suppression, and pathological hyperactivation. Understanding these compartment-specific regulatory mechanisms provides a framework for developing precision host-directed therapies aimed at enhancing antimicrobial immunity while limiting immunopathology, offering promising avenues for improved management of drug-sensitive and drug-resistant tuberculosis. - Source: PubMed
Publication date: 2026/08/11
Mehraj SafiyaAhmad Zahoor - Para-aortic paragangliomas (PGLs) are rare neuroendocrine tumors that may present with or without catecholamine hypersecretion. Their surgical management requires meticulous preoperative evaluation and careful intraoperative technique due to their proximity to major vascular structures. This report is novel in directly comparing functional and non-functional para-aortic PGLs, with an emphasis on perioperative strategy and surgical outcomes. - Source: PubMed
Publication date: 2026/06/26
Alqatta WailAl-Harethee Wasim