|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for ATP2A2(NM_170665.4) Search again
Product ID:
HQP150151
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ATP2B, DAR, DD, SERCA2
Gene Description:
ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 2
Target Gene Accession:
NM_170665.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
This gene encodes one of the SERCA Ca(2+)-ATPases, which are intracellular pumps located in the sarcoplasmic or endoplasmic reticula of muscle cells. This enzyme catalyzes the hydrolysis of ATP coupled with the translocation of calcium from the cytosol into the sarcoplasmic reticulum lumen, and is involved in regulation of the contraction/relaxation cycle. Mutations in this gene cause Darier-White disease, also known as keratosis follicularis, an autosomal dominant skin disorder characterized by loss of adhesion between epidermal cells and abnormal keratinization. Alternative splicing results in multiple transcript variants encoding different isoforms. [provided by RefSeq].
Gene References into function
- Evidence for calcineurin-mediated regulation of SERCA 2a activity in human myocardium
- A new splice variant is identified that is regulated during monocytic differentiation.
- multiple molecular mechanisms account for the plethora of pathologic states observed in Darier disease and provide evidence for the importance of SERCA2b dimerization in pump function in vivo.
- SERCA2a and phospholamban bind to S100A1 in the human heart
- Structure and transcriptional regulation of the SERCA2 gene.
- SERCA2b plays a key role in the biology of the epidermis, and its defects are sufficient to cause Darier's disease.
- kinetic analysis of SERCA1 and SERCA2 isoforms and the effects of mutation
- The coexistence of SERCA1 and -2, together with complex mixtures of MyHCs in most of the fibers provide the human EOMs with a unique molecular portfolio that allows a highly specific fine-tuning regimen of contraction and relaxation.
- TRAM2, as a part of the translocon, is required for the biosynthesis of type I collagen by coupling the activity of SERCA2b with the activity of the translocon
- distinct, heterozygous mutations (five missense, one nonsense, one deletion, and one insertion)in Darier's disease
- SERCA2b, a conformationally active protein with 11 membrane-spanning regions, loses function due to decreased conformational freedom in free cholesterol-ordered membranes
- ATP2A2 mutation found in a patient with severe Darier disease.
- combined influence of volume overload and age on atrial SERCA2a expression
- The combination of these histological and immunoblot results is consistent with the hypothesis that diaphragm remodeling elicited by severe COPD is characterized by a fast-to-slow SERCA isoform transformation.
- Three novel mutations in the ATP2A2 gene in Hungarian families with Darier's disease, including a novel splice site generating intronic nucleotide change.
- Although upregulated SERCA2a gene expression after support with a left ventricular assist device is independent of myopathic origin, normalization of myocardial force-frequency relationship is not.
- These results demonstrate the expression of the novel SERCA2c isoform in the heart and may point to a still unrecognized role of Plasma Memebrane Ca2+ ATPases in cardiomyopathies.
- SERCA1, 2, and 3 sensitivity to thapsigargin is dependent on a phenylalanine 256 to valine mutation
- new variants of the ATP2A2 gene in Darier's disease in Chinese patients
- This phenomenon correlates with the greater increase in [Ca2+]c induced by higher concentrations of thrombin, which further confirms that SERCA and PMCA activities are regulated by [Ca2+]c
- Reduced expression and downpregulation is found in acantholytic dermatoses.
- Preload stimulates SERCA expression. BNP antagonizes this mechanism. Inhibition of cGMP-dependent protein kinase restored preload-dependent SERCA upregulation in the presence of recombinant human BNP.
- Darier disease mutations in SERCA2b cause severe disruption of Ca2+ homeostasis by the defects in protein expression
- These findings put forward a novel consequence of compromised SERCA2 function in DD wherein up-regulation of TRPC1 augments cell proliferation and restrict apoptosis.
- ATP2A2 mutation found in a patient with severe Darier disease.
- SERCA 2b is a protagonist in prolactin-induced proliferation of prostate cells
- found abnormal expression of both PMCA and SERCA-type CA2+-ATPases in platelets of patients with adolescent idiopathic scoliosis
- These results indicate that the protein phosphatase-1/inhibitor-2 complex differentially regulates GSK3 dephosphorylation induced by KCl and that GSK3 activity regulates SERCA2 levels.
- Phospholamban in the human esophagus might be of less importance for regulation of SERCA than in heart. Lower expression of calsequestrin and calreticulin might contribute to increased lower esophageal sphincter pressure in achalasia.
- Germline alterations of ATP2A2 may predispose to lung and colon cancer: an impaired ATP2A2 gene might be involved directly or indirectly as an early event in carcinogenesis.
- In cells overexpressing SERCA2, the cyclic GMP-independent, redox regulation of SERCA2 cysteine-674 is required for the inhibition of cell migration by both exogenous and endogenously generated NO.
- In patients with COPD, SERCA2 concentration is reduced and the protein is tyrosine-nitrated in skeletal muscle from patients with low Body Mass Index compared to those with normal BMI.
- Either decreases in SERCA2a expression, increases in Na(+)/Ca(2+) exchanger (NCX) expression or elevated Na(+)(i) have been independently proposed as mediators of the negative FFR.
- results suggest a protective role of the A724A (c.2171G>A) polymorphism of ATP2A2 in subjects without hypertension
- Gene expression of ATP2A2 was studied in children with congenital heart defects.
- Histidine-rich Ca-binding protein may play a key role in the regulation of SR Ca cycling through its direct interactions with SERCA2 and triadin, mediating a fine cross talk between SR Ca uptake and release in the heart.
- The sarco(endo)plasmic reticulum Ca(2+) ATPase 2b (SERCA2b), which maintains high Ca(2+) concentration in the lumen of the endoplasmic reticulum, interacts specifically with the human delta opioid receptor.
- Sp1 plays an important and positive role in ATP2A2 gene expression in normal human keratinocytes in vivo and in vitro.
- The Japanese pedigree presented here has the same mutation, p.N767S, as three previously reported unrelated European families, establishing it as a common mutation in HDD.
- These results suggest that SERCA2b and 3 modulate thrombin-stimulated store-operated Ca(2+)entry probably by direct interaction with the hTRPC1 channel in human platelets.
- platelets from patients with type 2 diabetes mellitus, were found to have enhanced tyrosine nitration and inactivation of the sarcoplasmic endoplasmic reticulum Ca2+-ATPase (SERCA-2), elevated platelet [Ca2+]i, and activation of mu-calpain.
- These results indicate that failure of nitric oxide to inhibit migration in vascular smooth muscle cells exposed to high glucose is due to oxidation of the SERCA reactive cysteine-674.
- germline variants of the ATP2A2 genes might act as susceptibility alleles in head and neck squamous cell carcinoma
- reports two novel frame-shift mutations and a recurrent missense mutation in the central part of the ATP2A gene in three Chinese patients with Darier's disease
- SERCA activity is diminished in fibroblasts lacking both PS1 and PS2 genes, despite elevated SERCA2b steady-state levels.
- SERCA2 is an important target of FOG-2 and that increased FOG-2 expression may contribute to a decline in cardiac function in end-stage heart failure by impaired T3 signaling
- the increase in mechanical efficiency of cycling occurring during first weeks of endurance training may be due to down-regulation of SERCA pumps
- These findings suggest that HAX-1 may promote cell survival through modulation of SERCA2 protein levels and thus endoplasmic reticulum calcium stores.