PC_CB_W w. cap1
- Known as:
- PC_CB_W w. cap1
- Catalog number:
- 253375
- Product Quantity:
- 1
- Category:
- -
- Supplier:
- Herolab
- Gene target:
- PC_CB_W . cap1
Related genes to: PC_CB_W w. cap1
- Gene:
- CAP1 NIH gene
- Name:
- cyclase associated actin cytoskeleton regulatory protein 1
- Previous symbol:
- -
- Synonyms:
- CAP
- Chromosome:
- 1p34.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-07-17
- Date modifiied:
- 2017-05-17
Related products to: PC_CB_W w. cap1
Adenylyl Cyclase Associated Protein 1 (CAP1) Organism: Homo sapiens (Human) Source: Escherichia coliAdenylyl Cyclase Associated Protein 1 (CAP1) Organism: Homo sapiens (Human) Source: Escherichia coliAdenylyl Cyclase Associated Protein 1 (CAP1) Organism: Homo sapiens (Human) Source: Escherichia coliAdenylyl cyclase-associated protein 1,ASP-56 protein,CAP,CAP 1,CAP1,Pig,Sus scrofaAdenylyl cyclase-associated protein 1,Bos taurus,Bovine,CAP 1,CAP1Adenylyl cyclase-associated protein 1,CAP,CAP 1,CAP1,Homo sapiens,HumanAdenylyl cyclase-associated protein 1,Cap,CAP 1,Cap1,Mch1,Rat,Rattus norvegicusAdenylyl cyclase-associated protein 1,Cap,CAP 1,Cap1,Mouse,Mus musculusAnserine Adenylyl Cyclase Associated Protein 1 Elisa Kit (CAP1)Anserine anti - Adenylyl Cyclase Associated Protein 1 Elisa Kit (CAP1)anti-CAP1anti-CAP1anti-CAP1anti-CAP1anti-CAP1 Related articles to: PC_CB_W w. cap1
- Pulmonary capillary endothelial cells (ECs) form a highly specialized vascular interface that sustains gas exchange and organismal survival across species. Recent advances in single-cell transcriptomics and lineage tracing have revealed substantial heterogeneity within the pulmonary endothelium, redefining traditional views of capillary structure and function. In the adult lung, two major capillary populations: general capillary ECs (CAP1) and aerocyte capillary ECs (CAP2), have been identified, with CAP1 cells increasingly recognized as a heterogeneous and functionally diverse compartment that includes EC progenitors and reparative subpopulations. Emerging datasets further demonstrate arterial-venous polarization within the capillary bed and reveal gradients of gene expression that extend from macrovascular arteries and veins into the alveolar microvasculature. Within this polarized CAP1 landscape, several transcriptionally distinct EC subsets exhibit enhanced angiogenic potential and may contribute to EC regeneration during injury. This review synthesizes current knowledge of pulmonary capillary EC heterogeneity, emphasizing arterial-venous polarization of the capillary network, and the identification of reparative EC progenitors within the CAP1 population. We highlight emerging technologies including EC enrichment strategies, and transcriptomics, and epigenomic profiling that are beginning to resolve rare EC states and functional niches within the alveolar microvasculature. A deeper understanding of capillary EC diversity and lineage dynamics will be essential for identifying therapeutic targets aimed at restoring vascular stability, promoting regenerative angiogenesis, and preserving gas exchange in aging lungs and chronic lung diseases. - Source: PubMed
Publication date: 2026/06/02
Majka Susan MNiethamer Terren KCaporarello NunziaThorndyke Hannah FClair GeremyWest James DKarmouty-Quintana HarryAlvira Cristina M - Aberrant mitochondrial dynamics in podocytes are closely associated with the progression of diabetic nephropathy (DN); however, the underlying mechanisms remain incompletely understood. Recent research has demonstrated that cyclase-associated protein 1 (CAP1), an actin-binding protein, mediates mitochondrial fission. Therefore, we aimed to explore the regulatory role and mechanisms of CAP1 in high glucose (HG)-induced mitochondrial dysfunction in podocytes. CAP1 knockout reduced the severity of glomerular injuries and curtailed mitochondrial fission in podocytes in streptozotocin (STZ)-induced DN models. Subsequently, we observed that HG levels induced the mitochondrial translocation of CAP1 in podocytes, and CAP1 inhibition mitigated excessive mitochondrial fission. Mechanistically, our findings demonstrate that CAP1 facilitates HG-induced mitochondrial fission in podocytes by modulating actin reorganization. Furthermore, we present evidence that CAP1 interacts with Cofilin1, and this interaction plays a role in enhancing HG-induced mitochondrial fission in podocytes. This study elucidates the critical role of CAP1 in facilitating HG-induced mitochondrial fission in podocytes by regulating actin dynamics. These findings offer novel insights for the prevention and treatment of DN. - Source: PubMed
Publication date: 2026/06/01
Ma HuiminYao ShuangWang ZihanYu XinyingLi ZongdaZhang RuiLiang HaihaiJiao Jundong - Platelets are key mediators of hemostasis and thrombosis. Acid-sensing ion channel 3 (ASIC3), a proton-gated cation channel, can be activated at neutral pH by the synthetic compound 2-guanidine-4-methylquinazoline (GMQ). However, the role of GMQ in platelet activation and its potential dependence on ASIC3 remain unclear. This study investigated whether GMQ modulates platelet function at physiological pH (7.4), whether this regulation is mediated by ASIC3, and what the underlying molecular mechanisms are. We found that GMQ significantly suppressed platelet activation in both human and murine platelets at pH 7.4 and attenuated thrombus formation and hemostatic function in mice. ASIC3 was confirmed to be functionally expressed in human and murine platelets. Although ASIC3 deficiency did not affect basal platelet characteristics or platelet activation at pH 7.4, it markedly diminished GMQ-mediated suppression of platelet activation, thrombosis, and hemostasis. Mechanistically, GMQ enhanced cyclic adenosine monophosphate (cAMP) production and promoted protein kinase A (PKA) Thr197 phosphorylation through interaction with ASIC3-cyclase-associated protein 1 (CAP1), thereby suppressing platelet function. Overall, this study demonstrates, for the first time, that GMQ inhibits platelet activation and thrombosis under physiological pH by targeting ASIC3 and activating the CAP1/cAMP/PKA signaling pathway. These findings suggest that targeting the non-proton domain of ASIC3 at physiological pH may represent a novel and promising antiplatelet therapeutic strategy. - Source: PubMed
Publication date: 2026/05/30
Zhang PengLiu PengYu HanwenLiu DongshengWei MengZhang KandiHuang JianpengLi YingSu YuanyuanZhang TiantianZhang Junfeng - Visualizing synthetic labelled mRNAs in cells and animals enables the study of mRNA functions/dynamics and also helps to evaluate the delivery, distribution, intracellular kinetics, and efficacy of mRNA-based therapeutics/vaccines. Current methods for synthesizing labelled mRNAs, suitable for and tracking, rely on tedious and strenuous post-transcription modification processes. Herein, we report a direct one-pot co-transcriptional synthesis of labelled cap1 mRNAs by employing a series of fluorescently tagged trinucleotide cap analogs. These synthesized and translatable mRNAs with a single labelled fluorescent tag at the 3' position of the ribose ring of the m7G cap enabled real-time tracking of mRNA in biological systems without the need for additional chemical modifications. Robust transcriptional yield, capping efficiency and transcript integrity were achieved by the standard enzymatic co-transcription protocol with these fluorophore-labelled mGpppNN trinucleotide analogues. These synthesized labelled mRNAs retained their translational competence and activity, as confirmed by protein expression assays in mammalian cells. Further, we demonstrated that mRNAs with these labelled caps allowed direct visualization of mRNA uptake, intracellular trafficking and localization, and biodistribution using fluorescence microscopy and whole-animal imaging in mouse models. This strategy streamlines the generation of functional and trackable mRNAs, providing a powerful tool for the study of mRNA function and dynamics, for further evaluating mRNA vaccines and therapeutic delivery systems. - Source: PubMed
Publication date: 2026/05/14
Yang ChouGuo ChenZhou YiqianLi SuyongLi MengjieXie YalinLiu YanhuiLu XinyuZhang LijunMo GuohengZhu WeiHou JinlinZhang Jiancun - As mRNA emerges as a versatile tool for treating a range of diseases, efficient and scalable production remains an ongoing challenge. Inefficient co-transcriptional incorporation of cap analogs and generation of double-stranded RNA impurities are two of the major challenges that can result in increased manufacturing costs and time, as well as increased immunogenicity and reduced therapeutic potency. In an effort to overcome these challenges, we engineered T7 RNA polymerase variants to enhance capping efficiency and reduce dsRNA generation. In this work, we screened 59 T7 RNA polymerase variants and identified multiple variants, most notably R632N and Q649L, that achieved higher capping efficiency and up to 90% reduction in dsRNA impurity without compromising mRNA integrity. mRNA generated by these engineered T7 RNA polymerase variants showed enhanced translation and reduced immunogenicity in and studies. Additionally, they were observed to generate functional, relatively low-immunogenic mRNA without requiring excessive amounts of cap analogs or additional purification steps. Use of such T7 RNAP variants may thus offer a potentially cost-effective strategy for commercial scale mRNA therapeutic manufacturing. - Source: PubMed
Publication date: 2026/03/20
Sanjeev AthulHannigan CaseyGarrity RyanKamalakkannan Dhinesh SrinivasanClendaniel VictoriaMantri ManiniGlass ZachKasiewicz Lisa NLeipheimer JayKhan ZuneraMizoguchi TaijiPeshdary VianSummers Caroline RBeuning Penny JCheng Christopher J