ADAP1
- Known as:
- ADAP1
- Catalog number:
- 001178A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ADAP1
Related genes to: ADAP1
- Gene:
- ADAP1 NIH gene
- Name:
- ArfGAP with dual PH domains 1
- Previous symbol:
- CENTA1
- Synonyms:
- GCS1L
- Chromosome:
- 7p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-10-03
- Date modifiied:
- 2014-11-19
Related products to: ADAP1
Related articles to: ADAP1
- Recently evidence has suggested that long non-coding RNAs (lncRNAs) play a pivotal role in the prognosis and treatment of leukemia. However, studies on their use in differentiation therapy of acute myeloid leukemia (AML) remain scarce. In this study, we found that AC098613.1 was significantly increased in differentiated THP-1 cells, while its expression was significantly lower in AML patients. Moreover, AC098613.1 overexpression inhibited proliferation and induced differentiation of THP-1 and HL-60 cells. Mechanistically, we found that AC098613.1 targeted cell division cycle 5-like protein (CDC5L) to increase its stability, thereby enhancing its abundance and nuclear localization, and promoted the transcription of ADP-ribosylation factor GTPase activating protein with dual PH domains 1 (ADAP1) and the expression of nardilysin (encoded by NRD1), which ultimately induced the differentiation of AML cells. We further demonstrated in vivo that AC098613.1 overexpression significantly inhibited tumor growth by affecting the stability of CDC5L and regulating the expression of ADAP1, NRD1 and cyclin-dependent kinase 1 (CDK1). The research demonstrates that AC098613.1 promotes AML cell differentiation by regulating the CDC5L/ADAP1/NRD1 axis, providing a new target for AML differentiation therapy. - Source: PubMed
Publication date: 2026/02/09
Jiang QinglingWang XiaotingYao HangWang JinceTang PeiyuLiang MingpengPan ZhaohaiLi BohanLin ChunhuaWu QinxuanWang QiZheng QiushengKuok Chiu-FaiLiu HongfuSun ChanggangLi Defang - Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a clinically heterogeneous disease lacking approved therapies. To assess genetic susceptibility toward a specific metabolic phenotype, we performed a genome-wide association study on plasma biomarker levels (mGWAS) in patients with ME/CFS ( = 875) and healthy controls (HCs) ( = 36,033). We identified 112 significant SNP-biomarker associations in ME/CFS, compared with 4,114 in HCs. Two SNPs specific to ME/CFS, mapping to and , were associated with phospholipids in extra-large very low-density lipoproteins (VLDLs) and total fatty acids, respectively. Genetic effects of VLDL associations were among the least correlated between ME/CFS and HCs. Heterogeneity tests found differential effects for several lipid traits at , and , which are involved in immune regulation. ME/CFS mGWAS summary statistics were decomposed to uncover shared genetic-metabolic patterns, where enrichment analysis highlighted pathways in lipid metabolism, neurotransmitter transport, and inflammation. These findings provide a genetic and molecular rationale for patient heterogeneity and suggest a polygenic predisposition in which many small-effect variants may jointly perturb metabolic mechanisms. - Source: PubMed
Publication date: 2025/12/03
Huang KatherineMuneeb MuhammadThomas NatalieSchneider-Futschik Elena KGooley Paul RAscher David BArmstrong Christopher W - ArfGAP, with dual PH domain-containing protein 1/Centaurin-α1 (ADAP1/CentA1), is a brain-enriched and highly conserved Arf6 GTPase-activating and Ras-anchoring protein. CentA1 is involved in dendritic outgrowth and arborization, synaptogenesis, and axonal polarization by regulating the actin cytoskeleton dynamics. CentA1 upregulation and association with amyloid plaques in the human Alzheimer's disease (AD) brain suggest the role of this protein in AD progression. To understand the role of CentA1 in neurodegeneration, we crossbred CentA1 knock-out (KO) mice with the J20 mouse model of AD. We evaluated AD-associated behavioral and neuropathological hallmarks and gene expression profiles in J20 and J20 crossed with CentA1 KO (J20xKO) male mice to determine the impact of eliminating CentA1 expression on AD-related phenotypes. Spatial memory assessed by the Morris water maze test showed significant impairment in J20 mice, which was rescued in J20xKO mice. Moreover, neuropathological hallmarks of AD, such as amyloid plaque deposits and neuroinflammation, were significantly reduced in J20xKO mice. To identify potential mediators of AD phenotype rescue, we analyzed differentially expressed genes between genotypes. We found that changes in the gene profile by deletion of CentA1 from J20 (J20xKO vs J20) were anticorrelated with changes caused by APP overexpression (J20 vs wild type), consistent with rescue of J20 phenotypes by CentA1 KO. In summary, our data indicate that CentA1 is required for the progression of AD phenotypes in this model and that targeting CentA1 signaling might have therapeutic potential for AD prevention or treatment. - Source: PubMed
Publication date: 2025/11/25
Szatmari Erzsebet MMoran CoreyCohen Sarah JBashtovyy DenysJacob AmandaBunner WyattPhipps MaryLora Joan CristinoStackman Robert WYasuda Ryohei - Cardiomyocyte hypertrophy is regulated by several factors, including the ADP-ribosylation factor (Arf) family of small G proteins, among others. For instance, ArfGAP with dual pleckstrin homology domains 1 (Adap1) exerts an anti-hypertrophic effect in cultured cardiomyocytes. Its homologous protein, Adap2, is also expressed in the heart but its role remains elusive. To elucidate its function, we investigated the effects of adenoviral-mediated overexpression of Adap2 in cultured neonatal rat ventricular myocytes under both basal and pro-hypertrophic conditions, employing a range of microscopy and biochemical techniques. Despite minimal detection in neonatal rat hearts, Adap2 was found to be well expressed in adult rat hearts, being predominantly localized at the membrane fraction. In contrast to Adap1, overexpression of Adap2 provokes the robust accumulation of β1-integrin at the cellular surface of cultured cardiomyocytes. Interestingly, overexpressed Adap2 relocalizes at the sarcolemma and increases the size of cardiomyocytes upon phenylephrine stimulation, despite attenuating Erk1/2 phosphorylation and gene expression. Under these same conditions, cardiomyocytes overexpressing Adap2 also express higher level of detyrosinated tubulin, a marker of hypertrophic response. These findings provide new insights into the pro-hypertrophic function of Adap2 in cardiomyocytes. - Source: PubMed
Publication date: 2025/08/06
Berthiaume JonathanDumont Audrey-AnnDumont LauralyneRoy Marie-FrédériqueGiguère HugoAuger-Messier Mannix - ArfGAP with dual PH domain-containing protein 1 (ADAP1), also known as Centaurin alpha-1 (CentA1), is an actin-binding protein highly expressed in the central nervous system (CNS) that was previously shown to regulate dendritic spine density and plasticity. In the context of disease, ADAP1/CentA1 has been linked to Alzheimer's disease (AD) pathogenesis, cancer progression, and human immunodeficiency virus (HIV) reactivation. Here, we document that ADAP1/CentA1 is also mechanistically involved in CNS autoimmunity. We show that ADAP1/CentA1 deficient mice exhibit partial resistance to developing experimental autoimmune encephalomyelitis (EAE), an in vivo disease model recapitulating several features of multiple sclerosis (MS) pathogenesis. MS is a chronic autoimmune disorder of the CNS characterized by focal immune cell infiltration, demyelination, and axonal injury. Its etiology is still elusive, but genetic and environmental factors contribute to disease risk. By combining detailed immunophenotyping and single-cell RNA sequencing (scRNA-seq), we demonstrate that ADAP1/CentA1 is necessary for mounting a sufficient autoimmune response for EAE initiation and progression. In particular, the current study highlights that ADAP1/CentA1 expression in the immune system mainly targets the functioning of regulatory T cells (Tregs), monocytes, and natural killer (NK) cells. In summary, our study defines a novel function for ADAP/CentA1 outside of the CNS and helps elucidate the early molecular events taking place in the peripheral immune system in response to encephalitogenic challenges. - Source: PubMed
Carver Jonathan JBunner Wyatt PDenbrock Rachael RYin ChanghongHuang WeihuaSzatmari Erzsebet MDidonna Alessandro