ABI-1
- Known as:
- ABI-1
- Catalog number:
- PA1001
- Product Quantity:
- 100μg
- Category:
- -
- Supplier:
- SDlabs
- Gene target:
- ABI-1
Related genes to: ABI-1
- Gene:
- ABI1 NIH gene
- Name:
- abl interactor 1
- Previous symbol:
- SSH3BP1
- Synonyms:
- E3B1, ABI-1
- Chromosome:
- 10p12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-17
- Date modifiied:
- 2015-12-04
- Gene:
- ABI1P1 NIH gene
- Name:
- abl interactor 1 pseudogene 1
- Previous symbol:
- SSH3BP1P, ABI1P
- Synonyms:
- -
- Chromosome:
- 14q22.3
- Locus Type:
- pseudogene
- Date approved:
- 2003-01-13
- Date modifiied:
- 2018-05-23
Related products to: ABI-1
(I) LightCycler 1. 0; (Internal Control can't be used for this system) ; (II) LightCycler2. 0; (III) PE5700, MJ_Opticon etc. single color systems; (IV) ABI7000, ABI7300, ABI7500, ABI7900, ABI StepO96-Well Half Skirt PCR Plate for use on ABI-310096-Well Half Skirt PCR Plate for use on ABI-310096-Well Half Skirt PCR Plate for use on ABI-3100ABI Digital Vortex_Genie 2, 120VABI Digital Vortex_Genie 2, 120VABI Digital Vortex_Genie 2, 230V w_o plugABI Digital Vortex_Genie 2, 230V w_o plugABI gene family member 3-binding protein,ABI3BP,Homo sapiens,Human,Nesh-binding protein,NeshBP,NESHBP,Target of Nesh-SH3,Tarsh,TARSHABI-1Abi-1 (L201) pAb host: RabbitAbi-1 Antibody (OAAF05610)ABI-1 IHC AntibodyABI-1 IHC AntibodyABI-1 IHC Antibody Related articles to: ABI-1
- Non-heading Chinese cabbage (NHCC) is a highly economically valuable leafy vegetable widely grown in Asian regions. However, it undergoes rapid leaf yellowing and wilting during postharvest storage, which subsequently cause rapid quality decline and loss of nutritional components. Abscisic acid (ABA) promotes postharvest leaf senescence, while hydrogen-rich water (HRW) is widely used in postharvest preservation due to its excellent antioxidant properties; yet, the mechanism through which they interact to regulate postharvest senescence in NHCC remains unclear. Herein we found that exogenous HRW effectively delayed dark- and ABA-induced postharvest leaf senescence in NHCC, significantly maintained chlorophyll content, inhibited oxidative damage, and preserve nutritional components such as soluble sugars and vitamin C. The underlying mechanism was HRW inhibiting chlorophyll degradation by repressing the expression of chlorophyll catabolic genes like , , and . Meanwhile, HRW effectively lowered the accumulation of MDA and HO, elevated both the enzymatic activities and transcript abundance of and , and downregulated the transcript levels of , , , and , thereby maintaining reactive oxygen species (ROS) homeostasis. In addition, HRW negatively regulated ABA biosynthesis by inhibiting the transcript levels of , and , while promoting the transcription of , and . It also dampened the transcript abundance of ABA signaling components including , , and , thus blocking ABA signal transduction and alleviating its senescence-promoting effect. Collectively, this study confirms that HRW mitigates leaf senescence induced under dark and ABA conditions in NHCC via multiple synergistic pathways. - Source: PubMed
Publication date: 2026/04/27
Luo YongWang XinmanYin MengyaZhao RanzeZhang DingyuZhu Hongfang - Abscisic acid (ABA) is a major phytohormone regulating plant growth and stress responses. Subclass III SnRK2 kinases and clade A type 2C protein phosphatases (PP2Cs) are core components of ABA signaling. Despite advances from phosphoproteomics, major gaps remain, particularly in mapping PP2C dephosphorylation targets and SnRK2-dependent phosphorylation dynamics under non-stress conditions. Here, we performed large-scale LC-MS/MS phosphoproteomic analyses using the subclass III SnRK2 triple mutant and the constitutively active PP2C mutant , with and without ABA treatment in . We identified 2757 and 2886 differentially regulated phosphopeptides in and , respectively. Beyond known ABA signaling components, these datasets revealed numerous previously uncharacterized candidate proteins involved in metabolism, membrane transport, transcription, and cytoskeletal regulation. Integrative analysis uncovered a core set of candidate proteins oppositely regulated by SnRK2-mediated phosphorylation and ABI1-mediated dephosphorylation, defining a coordinated hierarchical network. These results indicate that the SnRK2-PP2C module functions not only in stress-induced ABA responses but also as a central regulator of phosphorylation homeostasis under basal conditions. This study provides a systematic framework for the global SnRK2-PP2C phosphorylation network and reframes ABA signaling as a dynamic homeostatic system. - Source: PubMed
Publication date: 2026/04/15
Takase HinanoSaigusa MizukiYamashita KotaUmezawa Taishi - Cardiovascular disease (CVD) is a major cause of morbidity/mortality in juvenile-onset systemic lupus erythematosus (JSLE), yet no reliable tools exist to stratify CVD-risk. - Source: PubMed
Publication date: 2026/03/26
Peng JunjieDönnes PierreMcDonnell ThomasArdoin Stacy PSchanberg Laura ELewandowski Laura BJury Elizabeth CRobinson George ACiurtin Coziana - Listeria monocytogenes (Lm), a prototypical intracellular bacterial pathogen, expresses ActA to initiate ARP2/3-mediated actin-based motility in the cytosol of host cells. Motile bacteria generate Lm-containing protrusions at the cell surface, facilitating direct cell-to-cell spread and dissemination within the host. Protrusion formation is an active, spatially regulated process, yet how Lm coordinates bacterial and host factors to orchestrate this process remains unclear. Here, we identify Abelson-interactor 1 (ABI1) as a host factor required for efficient Lm protrusion formation and cell-to-cell spread. Conditional knockout of Abi1 in mice significantly reduces susceptibility to Lm infection, while deletion of actA abrogates the protective effect of Abi1 knockout. During Lm infection, ABI1 is uncoupled from spectrin at the cell cortex and binds to EPS8 within protrusions. This ABI1 "complex switching" is initiated by the pore-forming toxin LLO, which perforates the host plasma membrane and triggers Ca influx, leading to calpain-mediated cleavage of the spectrin cytoskeleton. Spectrin cleavage mobilizes ABI1, allowing ABI1 to bind EPS8 and activate EPS8's actin capping activity to facilitate local actin recycling necessary for efficient protrusion elongation and cell-to-cell spread. These findings reveal an unrecognized host-pathogen interaction, in which a bacterial pore-forming toxin induces spatially confined cytoskeletal remodeling to promote cell-to-cell spread. - Source: PubMed
Publication date: 2026/04/13
Sun HeWizzard ArlonBrumell John HHiggins Darren E - The phytohormone abscisic acid (ABA) plays a pivotal role in plant growth, development, and stress responses. In the ABA signaling pathway, ABA-bound PYR1/PYL receptors form complexes with PP2Cs co-receptors, thereby releasing SnRK2 kinases from repression. However, the regulatory factors involved in the assembly of PYR1/PYLs-ABA-PP2Cs complexes remain poorly understood. In this study, by phenotypic and genetic analyses we show that the EAR-motif-containing adaptor protein (ECAP) is crucial for plant responses to ABA. We found that high ABA levels significantly upregulate ECAP expression. Biochemical assays unveiled that ECAP interacts with both ABA receptors (PYR1 and PYL1/3/11) and PP2Cs (ABI1/2), thus enhancing the formation of the PYR1-ABA-ABI1 complex and consequently exerting efficient inhibition on both the phosphatase activity and protein stability of ABI1. Furthermore, phosphatase activity assays revealed that ECAP binding can directly inhibit the phosphatase activity of ABI1/2 in a dose-dependent manner. Collectively, our results indicate that ECAP-mediated inhibition of PP2Cs relieves the suppression of SnRK2s, leading to ABA-responsive physiological effects, including the inhibition of seed germination and root growth, ABA-induced stomatal closure, and enhanced drought tolerance. This study identifies ECAP as a critical regulator in the ABA signaling pathway and elucidates its underlying mechanism, providing new insights into ABA-mediated plant development and stress responses. - Source: PubMed
Publication date: 2026/04/01
Li XingLi ChangjiangLv GaofengShi LeiTan ShulongLi XiLiu KaixiLi AnxingZhu LeiYang GuanghuiLi JigangFu Ying