sheep serum against human alpha_1 antichymotrypsin
- Known as:
- ovine blood serum H. sapiens alpha_1 antichymotrypsin
- Catalog number:
- ShAHu/AChy
- Product Quantity:
- 1 ml
- Category:
- -
- Supplier:
- Nordic Immunological Lab
- Gene target:
- sheep serum against human alpha_1 antichymotrypsin
Related genes to: sheep serum against human alpha_1 antichymotrypsin
- Gene:
- RALGAPA1 NIH gene
- Name:
- Ral GTPase activating protein catalytic alpha subunit 1
- Previous symbol:
- GARNL1
- Synonyms:
- GRIPE, DKFZp667F074, KIAA0884, Tulip1, RalGAPalpha1
- Chromosome:
- 14q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-10-09
- Date modifiied:
- 2018-11-19
- Gene:
- SERPINA1 NIH gene
- Name:
- serpin family A member 1
- Previous symbol:
- PI
- Synonyms:
- AAT, A1A, PI1, alpha-1-antitrypsin, A1AT, alpha1AT
- Chromosome:
- 14q32.13
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
- Gene:
- TMED11P NIH gene
- Name:
- transmembrane p24 trafficking protein 11, pseudogene
- Previous symbol:
- -
- Synonyms:
- p24alpha1, p24a1
- Chromosome:
- 4p16.3
- Locus Type:
- pseudogene
- Date approved:
- 2009-01-06
- Date modifiied:
- 2015-08-11
Related products to: sheep serum against human alpha_1 antichymotrypsin
Related articles to: sheep serum against human alpha_1 antichymotrypsin
- Sepsis accounts for nearly 20% of global mortality, with antibiotic resistance worsening clinical outcomes. Rapid antibiotic administration and accurate pathogen identification remain crucial. It is well now known that extracellular vesicles (EVs) from human cells and bacterial membrane vesicles (bMVs) play a central role in the interaction between host and pathogen and represent promising biomarkers for early infections. This study investigated how antibiotic exposure alters EV responses in Staphylococcus aureus (SA)spiked blood and compared these findings with EV proteome profiles from bacteremia patients. In an in vitro model, whole blood from healthy donors was spiked with SA at a multiplicity of infection (MOI) of 0.001, treated with clinically relevant concentrations of piperacillin-tazobactam, vancomycin, or moxifloxacin, and plasma was subsequently isolated for EV analysis. EVs were isolated using the Miltenyi Pan EV Kit and analyzed by bead-based flow cytometry and high-resolution LC-MS/MS. In parallel, serum EVs from healthy controls (n = 6) and bacteremia patients (n = 12; 6 blood culture-positive and 6 culture-negative) were analyzed using the same workflow. Flow cytometry revealed increased levels of CMO⁺ CD45⁺ PanEV⁺ SA⁺ vesicles in SA-spiked samples, particularly following low-dose piperacillin-tazobactam and high-dose vancomycin treatment, despite minimal changes in vesicle size and total particle counts. Proteomic analysis of plasma EVs showed significant alterations in protein composition, including increased abundance of the SA-derived ribosomal protein rplU and host defense-associated proteins. Functional enrichment highlighted pathways related to neutrophil degranulation, vesicle-mediated transport, and antibacterial responses. In patient samples, serum EVs were enriched in acute-phase and immune-related proteins, including SERPINA1, SERPINA3, CRP, and SAA2, along with canonical EV markers such as CD81 and syntenin-1, irrespective of blood culture status. Antibiotic exposure and SA infection are associated with measurable changes in the human EV proteome, characterized by enrichment of immune and host defense-related proteins despite stable vesicle numbers. Similar EV-associated protein patterns were observed in both blood culture-positive and -negative patient samples, reflecting shared features of the systemic host response to infection and highlighting the potential of EV profiling to capture infection-associated biological signals. - Source: PubMed
Publication date: 2026/05/30
Chiang Dapi MenglinPfaffl Michael WSchelling GustavMeidert Agnes SBrandes FlorianLudwig ChristinaWudy Susanne IKirchner BenediktYu Mia S CZenner ChristianUlbricht RosalieMuller LaurentReithmair Marlene - N-acetyltransferase 10 (NAT10) mediated N-acetylcytidine (acC) modification is a significant RNA modification in various tumors. This study aimed to investigate the underlying mechanism of NAT10 modulating the progression of colorectal cancer via mRNA acC modification. - Source: PubMed
Publication date: 2026/05/30
Fan WeicongMa Xinlei - Chronic obstructive pulmonary disease (COPD) is a progressive respiratory disorder influenced by both environmental and genetic factors. Variations in the SERPINA1 gene, particularly rs17580 (Glu288Val), may alter α₁-antitrypsin function and increase susceptibility to COPD. This study aimed to investigate the association of the SERPINA1 rs17580 variant with COPD progression using genetic and computational analyses. - Source: PubMed
Publication date: 2026/05/17
Qadir Muhammad FaizanJamal AdilIkhtiar FarhanZafar ImranBokhari Syed M Safeer Mehdi - Alpha-1 antitrypsin deficiency (AATD) is an inherited disorder caused by mutations in that result in insufficient circulating alpha-1 antitrypsin (AAT) and progressive lung and liver diseases. Adeno-associated virus (AAV)-mediated gene therapy offers the potential for durable AAT expression; however, achieving therapeutic serum concentrations (≥11 µM) at clinically acceptable vector doses remains a major challenge. Here, we evaluated multiple AAV vector design strategies to enhance AAT expression and increase vector potency, thereby reducing the required dose to levels below those associated with severe adverse events. Using AAV1- and AAV8-based platforms, we compared promoter and enhancer configurations, codon optimization of the transgene, single-stranded versus self-complementary vector genomes, alternative polyadenylation signals, and an engineered oxidation-resistant AAT variant. Across mouse and ferret models, the chicken β-actin expression cassette consistently produced higher AAT levels than a liver-specific promoter variant despite comparable vector biodistribution, reflecting superior intrinsic transcriptional activity or an important contribution. Codon optimization did not enhance expression and, in some cases, modestly reduced AAT levels. Self-complementary AAV vectors exhibited reduced overall expression due to required promoter truncation, yielding lower transgene output than full-length single-stranded constructs. Modifications to polyadenylation signals or enhancer combinations did not improve expression. An oxidation-resistant AAT variant resulted in lower circulating levels but may retain therapeutic potential through enhanced functional stability. Collectively, these findings demonstrate that promoter strength and cassette architecture are dominant determinants of AAV-AAT potency and that full-length, single-stranded vectors with robust regulatory elements provide the highest expression. This work defines key parameters governing AAT expression and provides a foundation for next-generation AAV designs aimed at achieving therapeutic efficacy at safer, lower vector doses for the treatment of AATD. - Source: PubMed
Publication date: 2026/05/20
Tang QiushiPires-Ferreira DeboraMueller ChristianGruntman Alisha MFlotte Terence R - Alpha-1 antitrypsin deficiency (AATD) is an autosomal codominant disorder caused by pathogenic variants in the gene, resulting in reduced circulating alpha-1 antitrypsin (AAT) or production of dysfunctional protein. AAT is the principal inhibitor of neutrophil elastase, and its deficiency leads to unchecked proteolytic activity, progressive destruction of lung parenchyma, and increased susceptibility to infections. Severe deficiency, particularly in individuals homozygous for the Z allele (PI*ZZ), predisposes to early-onset panacinar emphysema, chronic airflow obstruction, and liver disease. Despite its clinical relevance, AATD remains markedly underdiagnosed and is frequently misclassified as smoking-related chronic obstructive pulmonary disease (COPD), delaying access to disease-modifying therapy, genetic counselling, and preventive strategies. Early recognition is therefore essential to improve outcomes. We report the case of a 68-year-old ex-smoker with a long-standing diagnosis of "COPD" who presented with acute-on-chronic type 2 respiratory failure and community-acquired pneumonia. Spirometry revealed severe airflow obstruction, and high-resolution computed tomography demonstrated extensive basilar panlobular emphysema, raising suspicion for AATD. Serum AAT concentration was critically low at 26.8 mg·dL, and isoelectric focusing confirmed a PI*ZZ phenotype. Next-generation sequencing identified homozygosity for the c.1096G>A (Z) variant, with no additional pathogenic alleles. Cascade family screening revealed multiple heterozygous PI*MZ relatives. Before augmentation therapy could be initiated, the patient developed severe Legionella pneumophila pneumonia with secondary bacterial superinfection, progressing to refractory septic shock and death. This case illustrates how AATD can masquerade as smoking-related COPD for years, leading to missed opportunities for timely intervention. It underscores the importance of testing all adults with COPD or refractory asthma at least once, regardless of age or smoking history. Early diagnosis enables initiation of augmentation therapy, targeted vaccination, lifestyle modification, and genetic counselling, ultimately improving prognosis and reducing preventable morbidity and mortality. - Source: PubMed
Publication date: 2026/04/28
Ragnoli BeatricePochetti PatriziaVeselagu XheniMalerba Mario