ASAP3 antibody
- Known as:
- ASAP3 (anti-)
- Catalog number:
- orb100490
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- ASAP3 antibody
Related genes to: ASAP3 antibody
- Gene:
- ASAP3 NIH gene
- Name:
- ArfGAP with SH3 domain, ankyrin repeat and PH domain 3
- Previous symbol:
- DDEFL1
- Synonyms:
- FLJ20199, UPLC1, CENTB6
- Chromosome:
- 1p36.12
- Locus Type:
- gene with protein product
- Date approved:
- 2001-03-27
- Date modifiied:
- 2016-10-05
Related products to: ASAP3 antibody
Related articles to: ASAP3 antibody
- Esophageal squamous cell carcinoma (ESCC) is one of the most common malignancies worldwide. Despite advances in diagnosis and treatment, the lack of effective therapeutic targets continues to limit improvements in patient outcomes. ASAP3 has been implicated in tumor progression; however, its role and underlying mechanisms in ESCC remain unclear. - Source: PubMed
Publication date: 2026/06/12
Liu JingyuDai ChenluLiu LiJi MinMijiti GulirenaZhuang MengjieZhu SensenCheng MingLiu XuanmingZhang LinlinZhang WeiSu LipingPu Hongwei - Existing positively tuned ASAP-family voltage indicators such as ASAP4e exhibit superior photostability compared to the negatively tuned ASAP3 and ASAP5, but signal-to-noise ratios for spike detection remained similar to ASAP3. To improve spike detection by positively tuned ASAP indicators, we performed multiple rounds of structure-guided saturation mutagenesis of an ASAP4e predecessor while screening directly for faster responses. One variant, ASAP6c, demonstrated ~100% increases in fluorescence in response to single action potentials in both one-photon and two-photon imaging in vivo, achieving a 3-fold improvement in signal-to-noise ratios over ASAP4e. - Source: PubMed
Publication date: 2026/05/04
Lee SungmooZhang GuofengHao Yukun AlexRoth Richard HSun YueDong CanZhu JunGomez Laura CNatan Ryan GJiang DongyunLiu Lan XiangTesta-Silva GuilhermeHiramoto AtsukiRoska BotondFeldman DanielJi NaClandinin Thomas RGiocomo LisaDing JunLin Michael Z - The two-pore domain K channel TWIK1-related alkalinisation-activated K channel 2 (TALK-2) is encoded by KCNK17, which is one of the most abundant beta cell K channel transcripts that also shows high islet expression specificity. Polymorphisms that increase islet KNCK17 expression or result in TALK-2 gain-of-function are associated with a predisposition for developing type 2 diabetes. However, there is a gap in knowledge of the beta cell function(s) of TALK-2. As K channels typically control beta cell Ca handling, we aimed to examine the TALK-2 channel control of beta cell Ca homeostasis and the resulting impact on insulin secretion. - Source: PubMed
Publication date: 2026/02/25
Dobson Jordyn RDadi Prasanna KDickerson Matthew TNakhe Arya YBehera SomaGibson Shannon EPeachee Spencer JPiron AnthonyCnop MiriamJacobson David A - The electrical membrane voltage () characterizes the functional state of biological cells, thus requiring precise, noninvasive -sensing techniques. While voltage-dependent fluorescence intensity changes from genetically encoded voltage indicators (GEVIs) indicate changes, variability in sensor expression confounds the determination of absolute . Fluorescence lifetime imaging microscopy (FLIM) promises a solution to this problem, as fluorescence lifetime is expected to be unaffected by sensor expression and excitation intensity. By examining ASAP1, ASAP3, JEDI-1P, rEstus, and rEstus-NI (G138N:T141I) with one-photon-excited FLIM measurements, we demonstrate that all sensors display a voltage-dependent lifetime. Based on the highest lifetime change in the range of -120 to 60 mV, rEstus-NI (798 ps) and ASAP3 (726 ps) are preferred for FLIM recordings. At a physiologically relevant of -30 mV, the voltage sensitivity of rEstus-NI (6.6 ps/mV) is 3.6 and 1.4 times greater than that of ASAP1 and rEstus, respectively. As a proof of concept, we successfully used rEstus-NI to estimate absolute resting in HEK293T, A375 melanoma, and MCF7 breast cancer cells and quantified spontaneous fluctuations in A375 cells. - Source: PubMed
Publication date: 2025/11/22
Nair Anagha GopalakrishnanRodewald MarkoBae HyeonsooRühl PhilippPopp JürgenSchmitt MichaelMeyer-Zedler TobiasHeinemann Stefan H - The fourth leading cause of cancer-related death, pancreatic ductal adenocarcinoma (PDAC), has a 12% five-year survival rate. This disease has a poor prognosis and is characterized by a rigid stromal microenvironment, which represents a tangible challenge in its treatment. Chronic pancreatitis patients have a 10-fold greater risk of developing PDAC; in these patients, the ductal pH decreases from pH 8.0 to pH 6.0 due to bicarbonate insufficiency and the inflammatory milieu. Our goal was to understand the role of the acidic environment observed in chronic pancreatitis on oncogene expression in a pancreatic ductal cell line. Therefore, 80% confluent human pancreatic ductal epithelial cells were incubated at pH 6.0 to pH 7.2 for 6 h. Total RNA from the cells was processed to enrich the total mRNA in the samples. Gene expression was evaluated via next-generation sequencing (NGS) of biological replicates. RNA-seq analysis was carried out with the aid of an online tool, and the differentially expressed genes (FCs < ± 2.0) were identified; there were 90, 148, and 109 upregulated genes and 20, 14, and 23 downregulated genes at pH 6.0, 6.5, and 7.0, respectively. Four oncogenes were upregulated at pH 6.0, seven were upregulated at pH 6.5, and seven were upregulated at pH 7.0. The common genes that were upregulated at pH 6.0, pH 6.5, and pH 7.0 were lymphocyte cell-specific protein-tyrosine kinase (LCK) [pH 6.0, FC: 2.93; pH 6.5, FC: 2.93; pH 7.0, FC: 3.32], FGR proto-oncogene, Src family tyrosine kinase (FGR) [pH 6.0, FC: 4.17; pH 6.5, FC: 5.25; pH 7.0, FC: 5.09], and ArfGAP With SH3 domain, ankyrin repeat, and PH domain 3 (ASAP3) [pH 6.0, FC: 2.37; pH 6.5, FC: 3.84; pH 7.0, FC: 2.51]. The acidic environment triggers the activation of proto-oncogenes, which may trigger tumor initiation in chronic pancreatitis. - Source: PubMed
Publication date: 2025/04/11
Goudshelwar RenukaGalande SheethalRupula KarunaLakhtakia SundeepReddy D NageshwarSasikala Mitnala