MMAB 293T Cell Transient Overexpression Lysate(Denatured)
- Known as:
- MMAB 293T Cell Transient Overexpression Lysate(Denatured)
- Catalog number:
- H00326625-T02
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- MMAB 293T Cell Transient Overexpression Lysate(Denatured)
Related genes to: MMAB 293T Cell Transient Overexpression Lysate(Denatured)
- Gene:
- MMAB NIH gene
- Name:
- metabolism of cobalamin associated B
- Previous symbol:
- -
- Synonyms:
- cblB, CFAP23
- Chromosome:
- 12q24.11
- Locus Type:
- gene with protein product
- Date approved:
- 2003-02-11
- Date modifiied:
- 2018-08-02
Related products to: MMAB 293T Cell Transient Overexpression Lysate(Denatured)
Related articles to: MMAB 293T Cell Transient Overexpression Lysate(Denatured)
- Previously, we speculated that rabbits could produce more diverse and higher-affinity antibodies for small molecules due to their specific, unique antibody structure and antibody evolution mechanism. Here, using a single antibody-secreting cell (ASC) precise localization and sorting strategy, we discovered five rabbit monoclonal antibodies (RmAbs) with distinct recognition profiles to florfenicol (FF) and FF amine (FFA). Among them, RmAb-A4# exhibited superior performance, featuring high-affinity dual recognition of FF and FFA, with IC values of 0.07 ng/mL and 0.16 ng/mL in ELISA, demonstrating approximately 40-fold and 20-fold greater affinity compared to the best mouse monoclonal antibody (MmAb) 4F8 we previously reported, surpassing the reported antibodies derived from the mouse by 2-463-fold. As revealed by molecular docking and dynamic simulations, this enhancement is attributed to a more open binding pocket of RmAb-A4# and more hydrogen bonding interactions with FF and FFA. More importantly, RmAb-A4# displayed remarkable halotolerance (18-5000 mM NaCl) and enhanced pH stability (pH 4-9) in comparison to MmAb-4F8. Based on RmAb-A4#, a lateral flow immunoassay enabling rapid detection of FF and FFA was developed without pretreatment for milk and with a 3-fold dilution for eggs. The semiquantitative limit of detection reached 0.22 μg/L (FF) and 0.17 μg/L (FFA) in milk and 0.74 μg/kg (FF) and 0.78 μg/kg (FFA) in eggs. This work adopted a practical single ASC sorting strategy, discovered RmAb to small molecule, and validated its applicability for on-site sensitive immunoassay detection. - Source: PubMed
Publication date: 2026/06/03
Li PeipeiPan YantongLi YuanZhang YingjieLv BochenWen KaiYu XuezhiShen JianzhongWang Zhanhui - - Source: PubMed
Publication date: 2026/04/30
Voorhees Hannah MTaylor Jade LWesthoff MaartjeHell Johannes WDixon Rose ENieves-Cintrón MadelineMartín-Aragón Baudel MiguelNavedo Manuel F - Methylmalonic acidemia (MMA) is a recessive genetic disease caused by variants in the (mitochondrial enzyme methylmalonyl-CoA mutase) gene or by defects in transport or metabolism of MMUT cofactor (5' deoxyadenosylcobalamin), including variants in the gene. For the most recurrent pathogenic variant, c.556C>T (R186W), we identified a corrective editing strategy using adenine base editing. Deploying an adenine base editor mRNA and optimized hybrid guide RNA with lipid nanoparticles, we observed efficient corrective editing of the variant to wild-type, with minimized bystander editing and off-target editing in hepatocytes. These observations lay the groundwork for a gene editing therapy for patients with MMA resulting from at least one copy of the c.556C>T (R186W) variant, as well as a platform of similar therapies for patients with MMA caused by other variants amenable to adenine base editing. - Source: PubMed
Publication date: 2026/03/15
Kahn Elena MSaid HoodaQu PingAlameh Mohamad-GabrielWang XiaoMusunuru KiranAhrens-Nicklas Rebecca C - Recent studies show that genetic sequencing can not fully explain drug resistance in non-small cell lung cancer (NSCLC), suggesting undiscovered non-genetic mechanisms that can enable cancer cell survival. Propionate metabolism is the pathway by which odd-chain fatty acids, branched chain amino acids, and cholesterol are metabolized. We have previously shown that methylmalonic acid (MMA), a byproduct of propionate metabolism that accumulates when the pathway is disrupted, can activate epithelial-to-mesenchymal transition (EMT) in cell lines. But the clinical significance of propionate metabolism in cancer patients is not known. Here we show, for the first time, that propionate metabolism is dysregulated in patients with non-small cell lung cancer. MMA is elevated in lung tumors and in the serum of patients with metastatic NSCLC. Metabolism of cobalamin associated B (MMAB), a key regulatory gene of propionate metabolism, is downregulated in NSCLC and drug-tolerant persister cells, leading to MMA accumulation and EMT activation. We show that restoring expression of MMAB in NSCLC enhances targeted therapy and suppresses TGFβ signaling. These findings reveal propionate metabolism dysregulation as a non-genetic mechanism of drug resistance and highlight propionate metabolism as a potential therapeutic target. - Source: PubMed
Publication date: 2026/03/18
Parang BobakYoffe LironKhan RabiaLi ZhongchiNagiec Michal JGardner Eric EShieh YiweyHeise Rachel SSaxena AshishAltorki NasserBlenis John - : Isolated methylmalonic acidemia (iMMA) is a rare autosomal recessive metabolic disorder caused by defects in methylmalonyl-CoA mutase (MCM) activity or in the biosynthesis of its cofactor, adenosylcobalamin. Mutations in five genes-, , , , and -are known to underlie this condition. This study aimed to characterize the clinical features and molecular spectrum of iMMA in Malaysian patients of diverse ethnic backgrounds. : Patients with biochemical evidence suggestive of iMMA, including elevated propionylcarnitine (C3), increased C3/C2 ratio, and raised urine methylmalonic acid levels in the absence of hyperhomocysteinemia, were selected for genetic testing. Sanger sequencing was performed to identify pathogenic variants in the , , , , or genes. : The cohort consisted predominantly of Iban patients ( = 5), with the remaining cases comprising one Malay and one Thai-Malay individual. Age at diagnosis ranged from Day 1 of life to 6 years. All 7 patients were confirmed to have iMMA through molecular analysis. A total of seven pathogenic or likely pathogenic variants were identified, including two novel variants (c.246_250delinsGA and c.1358G>C), four known variants (c.560C>G, c.693C>G, c.982C>T, c.1106G>A), and one known variant (c.644+1G>A). Clinical presentation and disease severity varied across cases, reflecting underlying genotypic heterogeneity. : This study highlights the molecular diversity and clinical variability of iMMA in Malaysia. Our findings reinforce the importance of integrating metabolic screening with molecular diagnostics to identify disease-causing variants and guide patient management strategies effectively. - Source: PubMed
Publication date: 2026/03/03
Masri MardhiahKhalid NorzahidahSalleh NoornatishaLua Seok-HianAbdul Azize Nor AzimahYakob YusnitaAli Ernie ZuraidaMunusamy Vani A/PNgu Lock-HockLee Jeffrey Soon-YitToh Teck-HockHabib Anasufiza