goat serum against human alpha_1 antitrypsin
- Known as:
- caprine blood serum H. sapiens alpha_1 antitrypsin
- Catalog number:
- GAHu/Atr
- Product Quantity:
- 1 ml
- Category:
- -
- Supplier:
- Nordic Immunological Lab
- Gene target:
- goat serum against human alpha_1 antitrypsin
Related genes to: goat serum against human alpha_1 antitrypsin
- 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: goat serum against human alpha_1 antitrypsin
Related articles to: goat serum against human alpha_1 antitrypsin
- Individuals homozygous for the "Z" mutation with alpha-1 antitrypsin deficiency (AATD) are highly susceptible to emphysema. This predisposition has classically been attributed to a relative deficiency of circulating alpha-1 antitrypsin (AAT) reaching the lungs and associated protease-antiprotease imbalance. Accumulating evidence suggests that the presence of misfolded Z-AAT protein either in the circulation, the lung interstitium, or within resident lung cells could contribute to emphysema pathogenesis. We have shown that type 2 alveolar epithelial cells (AT2s), progenitor cells of the lung alveolus, heterogeneously retain Z-AAT and exhibit a transcriptional disease signature in AATD patient samples. However, a lack of model systems that faithfully recapitulate AT2 biology and associated Z-AAT expression has limited our ability to study this phenomenon. Here, we apply syngeneic induced pluripotent stem cell-derived AT2s (iAT2s) and a novel mouse model featuring AT2-specific inducible human expression to interrogate the cell-instrinsic consequences of Z-AAT expression, validating findings in an independent dataset of human COPD lung tissue comparing ZZ to MM genotypes. We find further evidence of Z-AAT retention within AT2s and identify shared AT2 transcriptomic disease signatures conserved across model systems, characterized by innate immune and inflammatory signaling, NF-κB activation, and endoplasmic reticulum stress. Mice with AT2-specific Z-AAT expression additionally demonstrate increased susceptibility to elastase-induced emphysema, providing functional evidence for AT2-intrinsic contributions to AATD-associated lung disease. Within iAT2s, a subpopulation of Z-AAT expressing cells exhibits activation of the PERK-eIF2α signaling axis and markers of an alveolar basal intermediate (ABI) state, emerging cell-autonomously in the absence of mesenchymal co-culture.Together, these data provide evidence that Z-AAT expression in AT2s induces heterogenous cell-intrinsic stress responses including proteotoxic stress, inflammatory signaling, and aberrant cell fate adoption, and is sufficient to result in predisposition to injury, supporting a potential contribution of AT2-intrinsic Z-AAT toxicity to human AATD-associated emphysema pathogenesis. - Source: PubMed
Publication date: 2026/04/08
Merritt CarlyGriffin Rose PAbo Kristine MKaserman Joseph EBawa Pushpinder SinghMartin Carlos VillacortaWang FeiyaMorley MichaelCho MichaelBasil Maria CSauler MaorWilson Andrew A - Contrast-induced acute kidney injury (CI-AKI) is a major cause of hospital-acquired AKI, but its molecular pathogenesis remains incompletely understood. In this study, we used quantitative 4D proteomics, integrating ion mass-to-charge ratio (m/z), retention time, ion intensity, and ion mobility, to profile renal tissues from a novel rat CI-AKI model based on renal venous congestion and contrast exposure, with sham-operated rats as controls. Differentially expressed proteins were identified and analyzed using pathway enrichment and protein-protein interaction (PPI) network approaches, followed by experimental validation. Using nominal screening criteria (|log2FC| ≥ 1.5 and < 0.05), we identified 180 candidate differentially expressed proteins, including 92 upregulated and 88 downregulated proteins. Pathway-level analyses showed coordinated upregulation of complement-related proteins, including C3/C5 convertase-related components and terminal pathway proteins, such as C9, together with a C4 isoform annotated as C4a in the reference database. Coagulation and fibrinolysis pathways were also markedly altered, including fibrinogen chains (FGA, FGB, FGG), PLAU, SERPINA1, and SERPINF2. In contrast, proteins associated with AMPK and MAPK signaling (including HNF4α, PRKAA2, PRKAB1, and MAP2K3) were reduced. These pathway-level changes were supported by RT-qPCR and immunohistochemical analyses. Collectively, our findings support a multidimensional injury network in rat CI-AKI involving complement activation, coagulation-fibrinolysis dysregulation, and impaired metabolic/stress-response signaling, and provide a proteomic resource for future mechanistic and translational studies. - Source: PubMed
Publication date: 2026/04/14
Yang QiangSun LimingZhang ZhijianYan ZhixinZhang JianHu JiachangDing Xiaoqiang - - Source: PubMed
Publication date: 2026/04/10
Åberg FredrikSemenova MariaLiukkonen VillePartanen JukkaHyvärinen KatiNordin Arno - Pyogenic liver abscess is an uncommon pediatric condition, and represents a rare causative agent in otherwise healthy children. Such infections may signal an underlying inborn error of immunity. Alpha-1 antitrypsin (A1AT), encoded by the gene, is a serine protease inhibitor with key immunomodulatory functions. In mouse models, A1AT prevents degradation of the antimicrobial SPLUNC1 protein to enhance host defense against . In humans, while A1AT variants can be associated with a generally increased risk of respiratory infection, to our knowledge no corresponding impact with respect to has been reported. - Source: PubMed
Publication date: 2026/03/27
Thomas SanyaD'Souza Alaric WAlhezam MusaabPlatt Craig DLevy Ofer - Acute myocardial infarction (AMI) ranks among the leading causes of death globally and is linked to obesity and the metabolism of lipids. The objective of this research was to develop an innovative predictive model utilizing obesity and lipid metabolism-related genes (OLMRGs) to facilitate the diagnosis and molecular typing of AMI. - Source: PubMed
Publication date: 2026/03/27
Li JianhuaXue ZixinZhang MinLu FengJi Shaoping