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
- The function of the NHS gene that is responsible for the Nance-Horan Syndrome has remained elusive at the cellular level. Using CRISPR/Cas9, we inactivated the NHS gene in MCF10A cells and characterized the isoforms expressed in these cells. NHS KO cells displayed reduced migration persistence, a phenotype that was fully rescued by the long isoform 1 (i1) that contains a N-terminal WAVE Homology Domain (WHD), but only partially rescued by the short isoform 2 (i2), which does not. Patient mutations resulting in NHS proteins truncated at their C-terminus also reduced the ability of NHS i1 to rescue migration persistence. Using Tandem Affinity Purification (TAP) of NHS i1 and mass spectrometry, we identified as major NHS partners, all subunits of the WAVE Regulatory Complex (WRC) except WAVE subunits themselves, indicating that the WHD of NHS assembles a WAVE Shell Complex (WSC). The Arp2/3 complex and the Nucleation Promoting Factor (NPF) WAVE that activates it are critical for migration persistence. To investigate the role of the NHS-containing WSC, we performed TAP of the ABI1 subunit in parental and NHS KO cells and identified differential partners associated with ABI1 only in parental cells, but not in NHS KO cells. The most abundant of these were the WIPF2/N-WASP complex, which together with the kinase ABL2, was also critical for migration persistence. These results suggest that NHS controls cell migration by remodeling NPF complexes and their higher order assembly. - Source: PubMed
Publication date: 2026/08/13
Tsydenzhapova EkaterinaFokin Artem IDavid Nicolas BRocques NathaliePolesskaya AnnaHaddad ImanVinh JoëlleGuérois RaphaëlGautreau Alexis M - Root vascular pathogens like (Fo) severely impact agriculture by colonizing the xylem, thereby disrupting the transport of water, nutrients, and signaling molecules within host plants. However, their effects on root growth and vascular development before xylem invasion, and the underlying molecular mechanisms, remain poorly understood. Here, we show that Fo triggers a rapid, systemic, abscisic acid (ABA) that seems to induce a developmental reprogramming in Arabidopsis that occurs prior to vascular colonization. This response is associated with root growth inhibition, disorganization of the root apical meristem, and alterations in xylem architecture. High-resolution imaging reveals that initial contact with Fo elevates root ABA levels, which parallels the modulation of key developmental pathways, including MIR165/PHB and VND7, which regulate vascular patterning and mediate premature xylem differentiation and remodeling. Phloem development is also affected, likely through disruption of CLE45-BAM3 signaling. Mutants impaired in endodermal ABA signaling, ELTPp::, and secondary wall formation, show constitutive elevated ABA levels, xylem defects, and enhanced resistance to Fo, suggesting that ABA-induced vascular remodeling contributes to the formation of structural barriers that limit infection. Additionally, Fo infection induces homogalacturonan demethylation in the stele, a modification associated with cell wall stiffening and reduced pathogen spread, which is constitutively observed in ELTPp::. Overall, our findings reveal ABA-mediated vascular plasticity, including cell wall remodeling as a developmentally encoded root defense mechanism. They highlight how transient hormonal cues reprogram root architecture to limit pathogen invasion and suggest strategies for crop protection. - Source: PubMed
Publication date: 2026/07/13
Aliaga Fandino Ana CeciliaPinto LucreziaSerrano AntonioSánchez-Rodríguez Clara - The Thr445Met substitution in the novel allele med25-5 uncouples seed dormancy from flowering, and MED25 acts as a negative regulator of seed dormancy via the DOG1 and ABA pathways. MED25, a pivotal subunit of the Mediator complex, regulates diverse biological processes, but its role in seed dormancy remains unclear. Here, we identified a novel MED25 allele, med25-5, harboring a Thr445Met substitution in the MD domain, which enhances seed dormancy without affecting flowering time in Arabidopsis thaliana. The med25-5 mutant exhibited increased dormancy with altered expressions in DOG1 and ABA signaling genes (e.g., ABI1, NHL6) and increased sensitivity to ABA and PAC. Either dog1-3 or abi3-10 can completely repress the enhanced seed dormancy of med25, indicating MED25 regulates dormancy requiring the DOG1 and ABA pathways. The Thr445 residue is conserved across crops, highlighting MED25's potential for crop improvement against pre-harvest sprouting. Our study uncovers MED25 as a negative regulator of seed dormancy, providing insights into the molecular mechanisms coordinating dormancy and flowering. - Source: PubMed
Publication date: 2026/07/02
Yang YueLi Xiao-YingDing RunCao HongLiu YongxiuLi Yu - Wiskott-Aldrich Syndrome Protein Family (WASF) members form a heteropentameric complex along with ABI1/2, NCKAP1, CYFIP1/2, and BRK1, termed the WASF Regulatory Complex (WRC), which regulates actin cytoskeletal remodeling. Upregulated WASF3 has been identified in pancreatic cancer and is associated with a poor prognosis, increased invasion, and metastasis. In this study, we sought to determine whether disruption of the WRC could suppress WASF3-mediated actin polymerization and subsequent cellular invasion and motility in pancreatic cancer cells. Here, we screened constrained peptides designed to disrupt the formation of the WRC at multiple protein-protein interfaces. The WASF3-derived constrained peptide WAHM1 was found to suppress cell motility and invasion in PANC-1 and BxPC-3 cells. Further, WAHM1 was found to permeate pancreatic cancer cell lines, bind to its protein targets in the WRC, and reduce WRC protein levels. WAHM1 may serve as a complementary strategy to downregulate WASF3-mediated migration and invasion in pancreatic cancer models. - Source: PubMed
Publication date: 2026/06/24
Dill Taylor CAlger Elliot JGambale SophiaKennedy Eileen J - 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