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anti-Human ATP2A2 Antibodies:
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Human Polyclonal ATP2A2 Primary Antibody for ChIP, IP - ABIN151703
Emter, McCune, Sparagna, Radin, Moore: Low-intensity exercise training delays onset of decompensated heart failure in spontaneously hypertensive heart failure rats. in American journal of physiology. Heart and circulatory physiology 2005
Show all 12 Pubmed References
Amphibian Monoclonal ATP2A2 Primary Antibody for FACS, ICC - ABIN152736
Asahi, Kurzydlowski, Tada, MacLennan: Sarcolipin inhibits polymerization of phospholamban to induce superinhibition of sarco(endo)plasmic reticulum Ca2+-ATPases (SERCAs). in The Journal of biological chemistry 2002
Show all 11 Pubmed References
Amphibian Monoclonal ATP2A2 Primary Antibody for BP, ELISA - ABIN152688
Sharp, McPherson, Dawson, Aoki, Campbell, Snyder: Differential immunohistochemical localization of inositol 1,4,5-trisphosphate- and ryanodine-sensitive Ca2+ release channels in rat brain. in The Journal of neuroscience : the official journal of the Society for Neuroscience 1993
Show all 16 Pubmed References
Human Polyclonal ATP2A2 Primary Antibody for IHC (p), WB - ABIN3044280
Guo, Zeng, Zhang, Zhang, Li, Wu, Guan, Liu, Zhang, Li, Wan: Extracellular matrix of mechanically stretched cardiac fibroblasts improves viability and metabolic activity of ventricular cells. in International journal of medical sciences 2013
Atp2a2/serca2 is found in a larger subset of cells, but is not ubiquitous as reported in adults.
the genomic organization and the equine ATP2A2 coding sequence and an association analysis for chronic pastern dermatitis using a sample of South German draft horses
SGK3 (show SGK3 Antibodies) a kinase transcriptionally regulated by estrogen receptor alpha (ERalpha (show ESR1 Antibodies)) in breast cancer, sustains ERalpha (show ESR1 Antibodies) signaling and drives the acquired aromatase (show CYP19A1 Antibodies) inhibitors resistance by protecting against endoplasmic reticulum (EnR (show LARGE Antibodies)) stress-induced ERalpha (show ESR1 Antibodies) downregulation and cell death through preserving SERCA2b function.
Darier disease (DD) is a rare autosomal dominant skin disorder due to mutations in the ATP2A2 gene.
SERCA2a gene transfer significantly improves left ventricle function and dimensions in doxorubicin-induced cardiomyopathy, suggesting LV-SERCA2a gene transfer an attractive treatment modality for doxorubicin-induced heart failure.
Studies indicate that Darier disease (DD) is caused by mutations in the ATP2A2 gene, whereas the ATP2C1 (show ATP2C1 Antibodies) gene is associated with Hailey-Hailey disease (HHD (show ATP2C1 Antibodies)).
Taken together, these results suggest that SERCA2 contributes to the migration of CCL21 (show CCL21 Antibodies)-activated Dendritic Cells as an important feature of the adaptive immune response and provide novel insights regarding the role of SERCA2 in Dendritic Cells functions.
VMP1 (show VMP1 Antibodies) modulates SERCA2 activity to control endoplasmic reticulum contacts for autophagosome formation.
The left atrium / right atrium expression ratio was significantly increased in Atrial fibrillation for SERCA2 - gene related to calcium uptake and release, and located on the sarcoplasmic reticulum membrane.
Loss of SERCA2 impairs ER-to-Golgi transport of nascent DC.
We propose that the increased SERCA1a (show ATP2A1 Antibodies) expression indicates the existence and location of compensating mechanisms in ischemic muscle.
Results show that ATP2A2 is variably expressed in astrocytoma tissues and its expression correlates with tumor grade. Its overexpression suppresses growth of astrocytoma cells.
Data suggest that the beneficial effects of SERCA2a gene transfer may involve the attenuation of ER stress-associated myocardial apoptosis.
Oxidative/nitrosative stress associated with lung resection influences SERCA2a activity independent of any influence on protein expression or phospholamban (show PLN Antibodies) phosphorylation.
overexpression of SERCA2a by in vivo rAAV1-mediated intracoronary gene transfer preserved systolic function, potentially prevented diastolic dysfunction, and improved ventricular remodeling.
Data show that rabbit cold tolerance is probably related to increased muscle oxidative metabolism and heat production by SERCA1 (show ATP2A1 Antibodies) and that these changes are not completely dependent on normal thyroid function.
These results indicate a mechanism relating SERCA1 (show ATP2A1 Antibodies) vicinal-cysteines oxidation to muscle fatigue.
Pin1 (show PIN1 Antibodies) serves as a modulator of SERCA2a and Na(2+)/Ca(2 (show CA2 Antibodies)+) exchanger 1 Ca(2 (show CA2 Antibodies)+) handling proteins, with loss of function resulting in impaired cardiomyocyte relaxation.
Pep2.5 prevented the down-regulation of SERCA2 expression in a) murine heart samples obtained from mice with sepsis and b) in cardiomyocytes exposed to serum from septic shock patients. Thus, we speculate that Pep2.5 may be able to prevent down-regulation of cardiac SERCA2 expression in patients with sepsis.
The findings support a salutary role of TLR9 (show TLR9 Antibodies) in some subsets of HF conditions and underline the importance for future studies on the mechanisms of TLR9 (show TLR9 Antibodies) in diastolic HF.
Our results indicate that changes in cell shape changed nuclear morphology and then the gene expression of IP3R1 (show ITPR1 Antibodies) and SERCA2, which produced different intracellular calcium transient patterns.
Nevertheless, the functional role of protein serotonylation in controlling SAN automaticity is largely unexplored. In this study, we screened the cardiomyocytes proteins and found that sarco(endo)plasmic reticulum Ca ATPase (show CA-P60A Antibodies) type 2a (SERCA2a) can be serotonylated. Simulation studies using mathematical SAN cell model showed that variation of Ca(2 (show CA2 Antibodies)+) affinity of SERCA2a pump cause either tachycardia or bradycardia.
Muscle RANK deletion had no significant effects on the sham or denervated slow-twitch soleus muscles. These data identify a novel role for RANK as a key regulator of Ca(2 (show CA2 Antibodies)+)storage and SERCA (show ATP2A3 Antibodies) activity, ultimately affecting denervated skeletal muscle function.
Generated were mice harboring N-ethyl-N-nitrosourea (ENU)-induced allelic mutations in Serca2: three missense mutations and one nonsense mutation. Mice harboring these Serca2 mutations developed tumors that were categorized as either early onset squamous cell tumors (SCT), with development similar to null-type knockout mice [2,4] (aggressive form; M682, M814), or late onset tumors (mild form; M1049, M1162).
Identify Atrap (show AGTRAP Antibodies) as a novel regulatory protein (show TGFB1 Antibodies) of the cardiac Ca(2+)-ATPase SERCA2a (show CA-P60A Antibodies). Suggest that Atrap (show AGTRAP Antibodies) enhances the activity of SERCA2a and, consequently, facilitates ventricular relaxation.
CAPN3 (show CAPN3 Antibodies) deficiency leads to degradation of SERCA (show ATP2A3 Antibodies) proteins and Ca2 (show CA2 Antibodies)+ dysregulation in the skeletal muscle.
SERCA2a gene transfer in the failing heart not only improves contractile function but also directly restores electric stability through amelioration of key arrhythmogenic substrate.
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.
Calcium ATPase at 60A
, ATPase, Ca++ transporting, cardiac muscle, slow twitch 2
, sarcoplasmic/endoplasmic reticulum calcium ATPase 2
, sarcoplasmic/endoplasmic reticulum calcium ATPase 2-like
, ATPase, Ca++ dependent, slow-twitch, cardiac muscle-2
, SR Ca(2+)-ATPase 2
, calcium pump 2
, calcium-transporting ATPase sarcoplasmic reticulum type, slow twitch skeletal muscle isoform
, cardiac Ca2+ ATPase
, endoplasmic reticulum class 1/2 Ca(2+) ATPase
, calcium ATPase
, sarcoplasmic reticulum Ca2+-transport ATPase isoform
, Ca(2+)-transport ATPase class 3
, sarcoplasmic/endoplasmic-reticulum Ca(2+) pump gene 2
, ATPase, Ca++ transporting, slow twitch 2
, sarco(endo)plasmic reticulum Ca(2+)-dependent ATPase 2
, sarco/endoplasmic reticulum Ca2+-ATPase 2
, sarcoplasmic reticulum slow-twitch Ca2 ATPase