G6PD Lyse Reagent
- Known as:
- Glucose-6-phosphate dehydrogenase Lyse Reagent
- Catalog number:
- G7583-LYS
- Product Quantity:
- 100 ml
- Category:
- -
- Supplier:
- Pointe scientific
- Gene target:
- G6PD Lyse Reagent
Related genes to: G6PD Lyse Reagent
- Gene:
- G6PD NIH gene
- Name:
- glucose-6-phosphate dehydrogenase
- Previous symbol:
- -
- Synonyms:
- G6PD1
- Chromosome:
- Xq28
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
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- An association between glucose-6-phosphate dehydrogenase deficiency (G6PDdef) and arterial stiffness has cross sectionally been reported in diabetic, but not in nondiabetic, subjects in Sardinia. The aims of the present longitudinal study were to evaluate: (1) sex differences in the influence of G6PDdef on trajectory of arterial stiffness; (2) the impact of hyperglycemia on trajectory of arterial stiffness; and (3) mechanistic pathways underlying this influence. - Source: PubMed
Publication date: 2026/04/29
Scuteri AngeloMorrell Christopher HOrru MarcoFiorillo EdoardoSestu AlessandroMarongiu MicheleGorospe MyriamLakatta Edward G - To explore the genetic factors contributing to unexplained infant jaundice and evaluate the significance of gene screening related to jaundice. - Source: PubMed
Publication date: 2026/04/13
Gao FangjianLi ShuyanChen YaliZhou YantingHu LiQiu Jianwu - Elevated phosphate (PO) levels in livestock wastewater (LSWW) significantly inhibit microalgal bioremediation, though the underlying mechanisms remain poorly characterized. This study investigated the physiological and molecular responses of microalgae to high PO stress at concentrations relevant to LSWW systems. Results demonstrated significant physiological stress and impaired nutrient uptake, with a 96.83% reduction in PO removal efficiency and a 62.28% reduction in removal rate. These responses resulted from a coordinated feedback inhibition, with enhanced intracellular phosphorus (P)-related metabolism but suppressed active PO transport. Specifically, stress adaptation was mediated through the coordinated upregulation of pentose PO pathway (e.g., genes encoding RBKS, rpiA, G6PD), glycolysis/gluconeogenesis (e.g., genes encoding talA, PFK, PFP) and phosphatidylinositol metabolism (e.g., genes encoding PIP5K, SAC1, IMPA, mmsA), collectively promoting NADPH regeneration, energy homeostasis, membrane transport, and cell signaling. ATP production was elevated through oxidative phosphorylation (e.g., genes encoding ppa and PMA1) whereas ATP conservation was achieved by downregulation genes encoding ABC transporters, despite concomitant oxidative stress and membrane destabilization. High PO suppressed key PO transporters genes (PHT1, PHT4, PHT5) and inhibited PO-dependent enzymatic activities, including acid phosphatase and ADP-glucose pyrophosphorylase. Photosynthetic integrity was maintained via carotenoid-mediated photoprotection, which mitigated oxidative damage through singlet oxygen quenching and radical scavenging. Metabolic profiling revealed a shift from protein and polysaccharide synthesis towards lipid accumulation, with notable production of odd-chain fatty acids exhibiting favorable biodiesel properties. These findings decipher the molecular regulatory networks underlying P stress in microalgae, providing practical strategies to enhance nutrient recovery and biomass valorization in microalgae-based LSWW treatment. - Source: PubMed
Publication date: 2026/04/25
Shan WenjuQiu ShuangBai JiaweiLi XiaofanWu ZhengshuaiBi QianGe Shijian - Glucose-6-phosphate dehydrogenase (G6PD) deficiency is among the most common inherited enzymatic disorders worldwide and is an important risk factor for neonatal hyperbilirubinemia. Regional data from Western Saudi Arabia based on universal newborn screening remain limited. To determine the prevalence of G6PD deficiency among newborns delivered at a tertiary center in Jeddah, Saudi Arabia, and to evaluate its association with clinically relevant outcomes, including early-onset jaundice (<24 h), need for phototherapy, admission for hyperbilirubinemia management, and readmission after discharge. We conducted a retrospective cohort study at King Abdulaziz Medical City, Western Region, Jeddah, Saudi Arabia, between January 2020 and May 2025. Cord blood samples from live-born infants were screened using a qualitative fluorescent spot test. Demographic variables (sex, gestational age, birth weight) and jaundice-related outcomes were extracted from the electronic medical record. Categorical variables were compared using chi-square testing, with < 0.05 considered statistically significant. : Among 14,964 screened newborns, 489 were identified as G6PD deficient, yielding a prevalence of 3.3%. Prevalence was higher in males than in females (5.6% vs. 0.9%). Among the G6PD-deficient infants, early-onset jaundice occurred in 17.2%, phototherapy was required in 36.0%, and 16.5% were admitted for hyperbilirubinemia management. Readmission for worsening jaundice requiring phototherapy occurred in 11.0%, and no exchange transfusions were required. Compared with term infants, late preterm infants had higher rates of early-onset jaundice (11/49, 22.4% vs. 73/440, 16.6%) and phototherapy use (22/49, 45.0% vs. 154/440, 35.0%) ( < 0.01). G6PD deficiency was identified in a substantial proportion of newborns in this large screened cohort and was associated with clinically significant jaundice-related outcomes, particularly among late preterm infants. These findings underscore the importance of universal screening and structured postnatal follow-up to reduce the risk of severe hyperbilirubinemia and its complications. Early identification of G6PD-deficient infants should be accompanied by careful bilirubin monitoring, clear discharge planning, and timely post-discharge follow-up, especially for those born late preterm. - Source: PubMed
Publication date: 2026/04/15
AlShugair RogayaAl-Qurashi MansourMustafa AhmadAlhindi Mohammad YAhmed AbrarAlNajjar HendAlDabbagh MonaSahafi AshrafAlmarzouki HashimAlRashdi Nabila AAlThobaiti Eman AAga Syed Sameer - Plasmodium vivax remains a challenge for malaria elimination in Nepal due to its ability to relapse. Radical cure with primaquine is effective but limited by poor adherence to the standard 14-day low-dose regimen. In 2022, the WHO recommended administering the same total dose (3.5 mg/kg) over 7 days to improve adherence. This study aimed to evaluate the 7-day low-dose primaquine regimen in G6PD-normal patients with uncomplicated P. vivax and/or P. falciparum malaria in the pre-elimination context of Nepal. - Source: PubMed
Publication date: 2026/04/25
Ghimire PrakashDahal GokarnaAdhikari NabarajRijal Komal RajAdhikari SanjibBanjara Megha RajMnjala HellenLee GrantWeston SophieRumaseb AngelaRai AnjanaLey BenediktHossain Mohammad SharifSimpson Julie ARajasekhar MeghaAdhikari BipinPrice Ric NLal Bibek KThriemer Kamala