ATP1a2 ELISA kit
- Known as:
- ATP1a2 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-ATP1a2-Mu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- ATP1a2 ELISA kit
Related genes to: ATP1a2 ELISA kit
- Gene:
- ATP1A2 NIH gene
- Name:
- ATPase Na+/K+ transporting subunit alpha 2
- Previous symbol:
- MHP2
- Synonyms:
- FHM2
- Chromosome:
- 1q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 1988-05-11
- Date modifiied:
- 2019-04-23
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- Chronic kidney disease is an increasing global public health concern, and the Developmental Origins of Health and Disease (DOHaD) concept proposes that adverse conditions during critical developmental windows predispose offspring to chronic disorders later in life. Maternal protein restriction (MPR), a well-established experimental model reflecting food insecurity, has been shown to impair nephrogenesis and promote long-term renal dysfunction. In this study, we investigated renal metabolic-epigenetic programming induced by gestational and lactational MPR in post-weaning male rats using a global kidney proteomic approach. MPR altered renal structure and profoundly dysregulated protein networks, characterized by downregulation of energy metabolism, ion transport, cytoskeletal organization, membrane integrity, and mitochondrial function, alongside upregulation of innate immune pathways, glutathione metabolism, vesicular trafficking, and cytoskeletal dynamics. Integrated pathway and disease enrichment analyses revealed the potential risk to hypertension, acid-base imbalance, renal tubular transport disorders, nephrosis, and renal failure. Key differentially expressed proteins (e.g., GPX1, CYCS, ATP1A2/ATP1B1, TUBB/TUBA isoforms, ANPEP, and metabolic enzymes) emerged as potential biomarkers of renal metabolic-epigenetic programming. Collectively, these findings identify molecular signatures that link early-life protein restriction to long-term risk of kidney disease and provide mechanistic insight into the nephron- and cell-specific consequences of MPR. - Source: PubMed
Publication date: 2026/05/07
Alvarez Danielle Amanda NizRibeiro Isabelle TenoriFioretto Matheus NaiaPires Marina PereiraBarata Luisa AnnibalMaciel Flávia AlessandraPortela Luiz Marcos FredianeMattos RenatoBaptista Hecttor SebastianVitali Pedro MenchiniFelipe Vinicius Alexandre AndradeFerreira Marcel RodriguesZambrano ElenaBoer Patrícia AlineJustulin Luis Antonio - Familial Hemiplegic migraine (FHM) is a rare migraine subtype characterised by transient unilateral motor weakness. Although familial forms are associated with variants in CACNA1A, ATP1A2, and SCN1A genes, many cases remain genetically unexplained, suggesting contributions from additional rare variations including single-nucleotide variants (SNVs) and copy-number variants (CNVs). - Source: PubMed
Publication date: 2026/04/24
Alfayyadh Mohammed MMaksemous NevenSutherland Heidi GLea Rodney AGriffiths Lyn R - Familial Hemiplegic Migraine (FHM) is a rare and severe subtype of migraine characterised by transient hemiparesis and aura symptoms. While pathogenic single-nucleotide variants (SNVs) have been studied extensively, the contribution of copy number variants (CNVs) to HM pathogenesis remains underexplored. Previous studies have primarily focused on known HM gene loci. This study presents the first whole-exome-wide comprehensive investigation of CNVs in HM, employing an integrative, multi-platform approach to identify CNVs present in cases with suspected FHM and to explore their potential biological relevance. We employed three independent bioinformatic tools for CNV detection: gCNV, CNVkit, and CNVPartition. gCNV was used to detect CNVs in 182 FHM cases and 500 UKBiobank (UKBB) non-neurological controls. CNVs identified by gCNV were then cross-validated using CNVkit and CNVPartition. Variants present in controls were excluded, and cross-platform concordance defined a finalised list of case-specific CNVs. Pathway enrichment analyses were also conducted to investigate the functional context of affected genes. We identified 27 high-confidence CNVs exclusively in the FHM cases, several intersecting with known pathogenic variants catalogued in ClinVar, including loci around the ATP1A2 gene and within the PRRT2 gene. MLPA validation confirmed a few gCNV calls. Enrichment analyses highlighted involvement of the Signalling by Rho GTPases and RNA Polymerase II Transcription pathways, suggesting mechanistic links to FHM pathogenesis. The identification of high-confidence, case-specific CNVs, including those impacting well-known FHM-associated genes such as ATP1A2 and PRRT2, advances our understanding of the genetic factors contributing to FHM. The enrichment of these CNVs in pathways related to Rho GTPase signalling and RNA Polymerase II transcription suggests new biological mechanisms underlying the disorder. These insights pave the way for improved genetic diagnosis and future research into targeted therapies for FHM. - Source: PubMed
Publication date: 2026/04/06
Alfayyadh Mohammed MZielke ThaisMaksemous NevenSutherland Heidi GLea Rodney AGriffiths Lyn R - Familial hemiplegic migraine (FHM) is a severe autosomal dominant subtype of migraine with aura, characterized by transient motor weakness during attacks. Known genes (CACNA1A, ATP1A2, SCN1A, PRRT2) account for fewer than 20% of genetically diagnosed cases. To identify novel genetic contributors to FHM, we performed whole-genome linkage analysis and partial exome sequencing in a four-generation pedigree. A candidate ion channel gene (SCN2A) was subsequently screened in six additional pedigrees with multiple affected members and in a cohort of 594 unrelated probands with familial or sporadic hemiplegic migraine without mutations in known FHM genes. Functional consequences of identified variants were assessed using heterologous expression and automated patch clamp recording. The neurophysiological impact of SCN2A dysfunction was investigated using computational neuron models. We identified a heterozygous missense mutation (c.4438A>G, p.Lys1480Glu) in SCN2A, encoding the neuronal voltage-gated sodium channel NaV1.2, which co-segregated with the FHM phenotype. Additional SCN2A variants (c.769T>A, p.Phe257Ile, and c.3955C>G, p.Arg1319Gly) were found in a second family and a sporadic case, respectively. All variants were absent from the gnomAD database. All ten individuals carrying a SCN2A variant experienced typical hemiplegic migraine attacks beginning in childhood. Two children heterozygous for p.Phe257Ile also had self-limited infantile seizures during the first year of life. None of the affected individuals exhibited permanent cerebellar ataxia, intellectual disability, or recurrent febrile coma. Functional studies revealed altered voltage-dependent and kinetic properties in all three variants that elicited abnormal action potential firing in a computer model of a neuron, supporting their pathogenicity. These findings implicate SCN2A dysfunction in both familial and sporadic hemiplegic migraine, expanding the genetic landscape of migraine and the phenotypic spectrum associated with SCN2A variants. - Source: PubMed
Publication date: 2026/03/26
Riant FlorenceThompson Christopher HWafa Syed M AFenton Timothy ADeKeyser Jean-MarcAbramova Tatiana VDesai Reshma RGazal StevenMoulin ThierryChaigne DenysKort LotfiCorpechot MichaelleTournier-Lasserve ElisabethBen-Shalom RoyGeorge Alfred LDucros Anne - In a recent article published in Nature Communications, Zheng et al. report that heightened stimulation of A receptors (ARs) located in epithelial cells of the chrorioid plexus (ChP) is responsible for the development of hydrocephalus (Zheng et al., Nat Commun 17:83, 2025). They show evidence in hydrocephalus patients and mice models of hydrocephalus that the cerebrospinal fluid (CSF) concentration of adenosine is raised to about threefold of the control value. Under pathological conditions, CSF adenosine levels may be increased in response to infection, hemorrhage, traumatic insults, and tumors, all of which are known to be the initiators of hydrocephalus. In careful experiments, performed mostly in mice models, established by the injection of autologous blood (imitation of hemorrhage) or kaolin (imitation of obstruction) to the cerebral ventricles, the production of CSF, the level of adenosine, and the expression of ARs was increased and in consequence the ventricles enlarged. The signaling mechanisms leading to increased production of CSF were then identified by the genetic knockdown of proteins that were assumed to be involved in this process. The AR-SPAK (SPS1-related proline/alanine-rich kinase)-PI3K (phosphoinositide 3 kinase)-Akt (protein kinase B)-NF-κB (a nuclear factor)-ATP1A2 (a Na,K-ATPase) pathway was suggested to be instrumental in hydrocephalus development. The clinically important conclusion deriving from this observation was that AR blockade by istradefylline, a Food and Drug Administration-approved drug could be introduced into the therapy of human hydrocephalus. - Source: PubMed
Publication date: 2026/03/25
Ren Xing-YingTang YongIlles Peter