ABI2
- Known as:
- ABI2
- Catalog number:
- 000955A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ABI2
Related genes to: ABI2
- Gene:
- ABI2 NIH gene
- Name:
- abl interactor 2
- Previous symbol:
- -
- Synonyms:
- ABI-2, AIP-1, ABI2B, AblBP3, argBPIA, SSH3BP2
- Chromosome:
- 2q33.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-11
- Date modifiied:
- 2016-10-05
Related products to: ABI2
Related articles to: ABI2
- Metastasis largely drives the high mortality of lung adenocarcinoma (LUAD), with anoikis resistance acting as a critical mediator in this process. This study aims to reveal the role and mechanism of ABI2 in anoikis resistance and LUAD metastasis. ABI2 expression levels and clinical value were analyzed using multiple databases. Functional studies were conducted in LUAD cells under attached or detached culture. The level of apoptosis was assessed by flow cytometry and Calcein-AM/EthD-1 staining. The metastasis ability was detected by transwell assay and lung metastasis model by tail vein injection. The ubiquitination effect of TRIM32 on ABI2 was analyzed by coimmunoprecipitation. This study revealed that ABI2 was significantly downregulated in LUAD tissues and anoikis-resistant LUAD cells. Functionally, ABI2 overexpression suppressed the anoikis resistance and LUAD metastasis, while ABI2 knockdown exerted the opposite effects. Mechanistically, ABI2 inhibited anoikis resistance by regulating epithelial-mesenchymal transition (EMT), thereby inhibiting tumor metastasis. EMT activation could rescue the effects of ABI2 on anoikis and metastasis. In addition, anoikis resistance modulated ABI2 ubiquitination by altering TRIM32 localization. Clinically, patients with low ABI2 and high TRIM32 experienced the worst prognosis in TCGA-LUAD. And a negative correlation between ABI2 and TRIM32 was further observed in both the public cohorts and the real-world cohort. In conclusion, ABI2 exerts tumor-suppressive effects in LUAD by inhibiting anoikis resistance and metastasis. The TRIM32‑ABI2‑EMT axis shows encouraging preclinical prospects, yet sufficient follow-up studies are indispensable to support its clinical therapeutic potential. - Source: PubMed
Publication date: 2026/06/25
Liu YongtingJiang ZhaohuiZhao YulongChen Qiong - Bacterial wilt, caused by Ralstonia solanacearum, poses a significant threat to global tomato production, underscoring the need for sustainable management strategies. In this study, we characterized a novel lipopeptide from Bacillus pumilus strain LP-823 and evaluated its efficacy against tomato bacterial wilt. Structural analysis using LC-QTOF MS/MS identified the lipopeptides as surfactin variants with fatty acid chains ranging from C to C, including C-C homologues not previously reported in this species. In pot experiments, treatment with LP-823 lipopeptides significantly suppressed disease development, delaying symptom onset by four days and reducing final disease incidence and disease index by 29.63% and 36.19%, respectively, at 20 days post-inoculation. The lipopeptides exhibited no direct antibacterial activity in vitro. Instead, they triggered plant-mediated defense responses, as evidenced by marked increases in phenylalanine ammonia-lyase (PAL) and polyphenol oxidase (PPO) activities, which peaked at 36 h post-treatment with 5.7-fold and 6.8-fold increases, respectively. Integrated transcriptomic and metabolomic analyses revealed that lipopeptide treatment orchestrates a multifaceted defense network, including modulation of ROS homeostasis (downregulation of AOX1a and CAT2), reprogramming of ABA signaling (upregulation of ABI2, downregulation of ZEP), suppression of aquaporin (PIP2-1) expression, and redirection of phenylpropanoid metabolism. These coordinated responses collectively explain the observed disease suppression and enhanced defense enzyme activities. Overall, our results establish the LP-823 lipopeptide as a potent elicitor of induced systemic resistance with considerable potential for the sustainable management of bacterial wilt in tomato. - Source: PubMed
Publication date: 2026/06/13
Chen ZhengFeng JunjieLin TaoXie DongjunWei HuiLin EnquanChen Meichun - Abscisic acid (ABA) is a fundamental regulator of plant development, growth, and drought adaptation, and it modulates the transition to flowering. However, the molecular mechanisms by which ABA delays flowering remain unclear. Recently, ABA INSENSITIVE 2 (ABI2), a core component of the ABA signaling pathway, was reported to positively regulate floral transition in . The expression of floral repressors such as and was strongly upregulated, whereas flowering promoting genes including , and were downregulated in the mutant. Moreover, ABI5 protein levels and phosphorylation status were enhanced in , suggesting that ABI2 reduces ABI5 activity and suppresses the activation of its target genes, such as . Genetic analyses revealed that ABI2 functions upstream of ABI5. In conclusion, these findings indicate that ABI2 is a major switch that fine-tunes the crosstalk between ABA signaling and floral transition in . - Source: PubMed
Publication date: 2026/06/06
Ali AkhtarZareen ShahPark JunghoonYun Dae-Jin - Drought stress affects crop yield and quality. Abscisic acid (ABA) plays a crucial role in plant responses to drought stress; however, the signal transduction mechanism in potato (Solanum tuberosum L.) remains unclear. This study identifies a WRKY transcription factor (TF) member, StWRKY46, that enhances drought tolerance in potato. Under drought, StWRKY46 binds directly to the promoter of StPYL1 (a PYR/PYL family ABA receptor) and activates its transcription, triggering the ABA signaling pathway and improving drought tolerance in potato. StPYL1 interacts with StHAB1, StPP2C24, StPP2C51.1, and StABI2. StABI2 acts as a key negative regulator of ABA signaling. It interacts with StOST1, StSnRK2.5, and StSnRK2.6 to regulate the expression of stomatal movement-related genes, including the slow-type anion channel 1 (StSLAC1) and guard cell hydrogen peroxide-resistant 1 (StGHR1), thereby potentiating ABA-induced stomatal closure. Overall, our findings demonstrate the molecular mechanism of StWRKY46-mediated drought tolerance through the ABA-StPYL1-StABI2-StOST1/StSnRK2.5/StSnRK2.6 pathway in potato. - Source: PubMed
Wei HanWang XiaoLi ShiguiZhang NingSi Huaijun - The modulation of plant responses to abscisic acid (ABA) and/or abiotic stresses can be manipulated by the expression of ABA-responsive genes, which is affected by phytohormone ABA. While some ABA-responsive genes have been shown to regulate plant responses to ABA and/or abiotic stresses, the functions of numerous ABA-responsive genes remain unknown. Therefore, characterizing these unstudied genes would provide a practical way to identify novel regulators of plant adaptations to ABA and/or abiotic stresses. Here, we characterized four closely related unstudied ABA-responsive genes in , named (). We found that ABA treatment induces expression level, and our results in transfected protoplasts show that AtAUGs exhibit nucleus localization and downregulate the co-transfected reporter expression level. The results of ABA sensitivity assays, including seed germination, cotyledon greening, and root extension assay show that transgenic plants overexpressing had increased sensitivity, but mutants generated by isolating T-DNA insertion lines or through CRISPR/Cas9 gene-editing of had decreased sensitivity; in addition, the greatest decrease in ABA sensitivity was observed in the () quadruple mutants. The qRT-PCR results show that the expression levels of several Type 2C Protein Phosphatase (PP2C) genes, the key negative regulator genes of ABA signaling including , (), , (), (), and () decreased in transgenic plants, but increased in the quadruple mutants. Taken together, these results suggest that are ABA-responsive genes, and AtAUGs positively regulate ABA responses in a redundant manner, by downregulating the expression of crucial negative regulator genes in ABA signaling. - Source: PubMed
Publication date: 2026/03/26
Wang XutongZheng KaijieSu RuqianWang WeiJing XiaoxiaoWang YatingWu YaowenCheng NiniChen SiyuWang Shucai