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anti-Mouse (Murine) ATP2A1 Antikörper:
anti-Rat (Rattus) ATP2A1 Antikörper:
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Human Polyclonal ATP2A1 Primary Antibody für FACS, IHC (p) - ABIN1881089
Salanova, Schiffl, Blottner: Atypical fast SERCA1a protein expression in slow myofibers and differential S-nitrosylation prevented by exercise during long term bed rest. in Histochemistry and cell biology 2009
Show all 3 Pubmed References
The different forms of phospholamban (zeige PLN Antikörper) in zebrafish may provide a novel SERCA regulatory mechanism.
study showed that accordian acc(dta5) mutants harbor a novel mutation in atp2a1; indicate the acc(dta5) mutation diminishes SERCA1 function to a greater degree than other acc alleles through haploinsufficient or dominant-negative molecular mechanisms
encodes the sarco(endo)plasmic reticulum Ca2+-ATPase 1 (SERCA1), a Ca2 (zeige CA2 Antikörper)+ pump found in the muscle sarcoplasmic reticulum (SR) that is responsible for pumping Ca2 (zeige CA2 Antikörper)+ from the cytosol back to the SR
concluded that the motility dysfunction in embryonic and larval accordion zebrafish stems directly from defective calcium transport in skeletal muscle due to mutation in SERCA rather than defective CNS drive.
Atp2a1/serca1 is expressed as soon as the end of gastrulation in a subset of the myod (zeige MYOD1 Antikörper)-positive cells, and later labels prospective slow muscle cells in the superficial part of the somite.
Cell functions regulated by protein-protein interactions of the SERCA1a-sarcolipin (zeige SLN Antikörper) complex is accomplished via s-palmitoylation and s-oleoylation of sarcolipin (zeige SLN Antikörper).
The changes in expression of SERCA1 potentially disturb the normal Ca2 (zeige CA2 Antikörper)+ channel as well as the balance of Ca2 (zeige CA2 Antikörper)+ homeostasis.
the major SR membrane lipid PC is optimal for all steps and, unlike the other headgroups, contributes favorable electrostatics and non-electrostatic elements during the Ca-ATPase (zeige CA-P60A Antikörper) transition
ATP-dependent Ca(2 (zeige CA2 Antikörper)+) transport by SERCA (zeige ATP2A3 Antikörper) in single giant unilamellar vesicles was detected directly using confocal fluorescence microscopy.
Here we describe the methods to analyze these processes in the transport cycle with a representative member of P-type ATPase (zeige ATP7A Antikörper) family, SERCA1a, sarco(endo)plasmic reticulum Ca(2+)-ATPase (zeige CA-P60A Antikörper)
oligonucleotide-based drugs could be used to fine-tune SERCA (zeige ATP2A3 Antikörper) function to counterbalance the extent of the pathological insults.
Inhibition of the sarco/endoplasmic reticulum Ca2+-ATPase (zeige ATP2A3 Antikörper) (SERCA1) by rutin derivatives.
Infrared spectroscopy was used to characterise recombinant sarcoplasmic reticulum Ca2+-ATPase (SERCA1a).
Data show that biselyngbyasides (BLSs) bind to the pump SERCA1a calcium ATPase (zeige CA-P60A Antikörper) near the cytoplasmic surface of the transmembrane region.
Rescue of mutated SERCA1 to sarcoplasmic reticulum membrane can re-establish resting cytosolic Ca(2 (zeige CA2 Antikörper)+) concentration and prevent the appearance of pathological signs of cattle pseudomyotonia
Conformation of the SERCA1A calcium ATPase (zeige CA-P60A Antikörper) in the presence of different lipids.
CAPN3 (zeige CAPN3 Antikörper) deficiency leads to degradation of SERCA (zeige ATP2A3 Antikörper) proteins and Ca2 (zeige CA2 Antikörper)+ dysregulation in the skeletal muscle.
Ebf3 (zeige EBF3 Antikörper) binds directly to the promoter of Atp2a1 and synergises with MyoD (zeige MYOD1 Antikörper) in the induction of Atp2a1
Formalin evokes calcium transients from the endoplasmatic reticulum via SERCA1-dependent, TRPA1 (zeige TRPA1 Antikörper)-independent mechanism that may underlie formaldehyde-induced pan (zeige SUPT6H Antikörper)-neuronal excitation and subsequent inflammation.
SERCA1b is considered to play an essential role in the regulation of [Ca2 (zeige CA2 Antikörper)+]i and its ab ovo gene silencing results in decreased skeletal muscle differentiation.
Data show that in healthy transgenic mice, cardiac-specific sarcoplasmic reticulum calcium ATPase (zeige CA-P60A Antikörper) SERCA1a expression increased active cell-surface glucose transporter GLUT4 (zeige SLC2A4 Antikörper) and glucose uptake in the myocardium.
Data suggest that the cardiac depressant properties of neuronostatin possibly associated with loss of sarcoplasmic reticulum Ca2+-ATPase SERCA (zeige ATP2A3 Antikörper) phosphorylation.
Results indicated that sine oculis homeobox (zeige PRRX1 Antikörper) 1 (Six1 (zeige SIX1 Antikörper)) overexpression could significantly promote the expression of fast-type muscle genes Atp2a1, Srl (zeige SRL Antikörper), and Mylpf (zeige MYLPF Antikörper).
Protein levels of CSQ1 (zeige CASQ1 Antikörper), SERCA1, and SERCA2 (zeige ATP2A2 Antikörper) are re-adjusted in skeletal muscles depending on the demands of diverse exercise training programs.
dystrophic phenotype observed in delta-sarcoglycan (zeige SGCD Antikörper)-null (Sgcd (zeige SGCD Antikörper)(-/-)) mice and dystrophin (zeige DMD Antikörper) mutant mdx (zeige DMD Antikörper) mice is dramatically improved by skeletal muscle-specific (zeige EIF3K Antikörper) overexpression of sarcoplasmic reticulum Ca(2+) ATPase 1 (SERCA1)
Sarcolipin (zeige SLN Antikörper) is a novel regulator of SERCA (zeige ATP2A3 Antikörper) pump activity, and its inhibitory effect can be reversed by beta-adrenergic agonists.
Study demonstrated that (a) the distribution and the expression levels of total SERCA1 and SERCA2 (zeige ATP2A2 Antikörper), the activity of SR Ca2+ ATPase, and the oligomerization of SERCA1 are similar in patients with myotonic dystrophy 1, myotonic dystrophy 2, hypothyroid myopathy and control subjects; and (b) SERCA1b is expressed in patients with myotonic dystrophy, mainly in myotonic dystrophy 2 muscles.
These results suggest that sAnk1 interacts with SLN (zeige SLN Antikörper) both directly and in complex with SERCA1 and reduces SLN's inhibitory effect on SERCA1 activity.
The sphingolipid sphingosine increases the [Ca(2 (zeige CA2 Antikörper)+)]i by inhibiting the sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA (zeige CA-P60A Antikörper)), in a similar manner to thapsigargin (Tg), a specific inhibitor of this Ca(2 (zeige CA2 Antikörper)+) pump.
Thus the human SERCA1b has a different expression pattern from that of rodents and it is associated with DM2 (zeige CNBP Antikörper).
We conclude that PLB (zeige PLN Antikörper) C-terminal residues are critical for localization, oligomerization, and regulatory function. In particular, the PLB (zeige PLN Antikörper) C terminus is an important determinant of the quaternary structure of the SERCA (zeige ATP2A3 Antikörper) regulatory complex.
Aberrant splicing of SERCA1 may alter intracellular Ca(2 (zeige CA2 Antikörper)+) signalling in myotonic dystrophy 1 and 2 myotubes. The differing dysregulation of intracellular Ca(2 (zeige CA2 Antikörper)+) handling in DM1 (zeige DMPK Antikörper) and DM2 (zeige CNBP Antikörper) may explain their distinct sarcolemmal hyperexcitabilities.
We performed a detailed study of SERCA1 protein expression in muscle of patients with BD and BS, and evaluated the alternative splicing of SERCA1 in primary cultures of normal human muscle
These results indicate that PKC signaling is involved in the splicing of SERCA1 and provide new evidence for a link between alternative splicing and PKC signaling.
Results demonstrate that a cattle congenital pseudomyotonia is caused by a SERCA1 deficiency, resulting from a defect in the ATP2A1 gene
crystal structure of SERCA (zeige ATP2A3 Antikörper), crystallized in the E1 conformation and determined at 2.9A resolution
Mutation in ATP2A1 is associated with congenital muscular dystony type 1
study reports the identification of a missense mutation in ATP2A1 in congential pseudomytonia of Chianina cattle; mutation analysis of ATP2A1 exons revealed a perfectly associated missense mutation in exon 6 (c.491G>A) leading to p.Arg164His substitution
In this study, we provide biochemical evidence for a selective deficiency in SERCA1 protein levels in sarcoplasmic reticulum membranes from Chianina cattle with congenital pseudomyotonia
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 to the sarcoplasmic reticulum lumen, and is involved in muscular excitation and contraction. Mutations in this gene cause some autosomal recessive forms of Brody disease, characterized by increasing impairment of muscular relaxation during exercise. Alternative splicing results in two transcript variants encoding different isoforms.
ATPase, Ca++ transporting, fast twitch 1
, sarcoendoplasmic reticulum calcium ATPase
, ATPase, Ca++ transporting, cardiac muscle, fast twitch 1
, ATPase, Ca++ transporting, cardiac muscle, slow twitch 2
, sarcoplasmic/endoplasmic reticulum calcium ATPase 1-like
, ATPase, Ca++ transporting, slow twitch 2
, sarcoplasmic/endoplasmic reticulum calcium ATPase 1
, ATPase, Ca++ transporting, ubiquitous
, SR Ca(2+)-ATPase 1
, calcium pump 1
, calcium-transporting ATPase sarcoplasmic reticulum type, fast twitch skeletal muscle isoform
, endoplasmic reticulum class 1/2 Ca(2+) ATPase