Recombinant Mouse Protein S100-A1 (S100a1)

Code
MSDS	MSDS Datasheet
Size	Pls inquire
Source
Conjugate
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Product Details
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Target Background

Product Details

Purity

>85% (SDS-PAGE)

Target Names

S100a1

Uniprot NO.

P56565

Species

Mus musculus (Mouse)

Source

Yeast

Expression Region

2-94

Target Protein Sequence

GSELESAME TLINVFHAHS GQEGDKYKLS KKELKDLLQT ELSGFLDVQK DADAVDKVMK ELDENGDGEV DFKEYVVLVA ALTVACNNFF WETS
Note: The complete sequence may include tag sequence, target protein sequence, linker sequence and extra sequence that is translated with the protein sequence for the purpose(s) of secretion, stability, solubility, etc.
If the exact amino acid sequence of this recombinant protein is critical to your application, please explicitly request the full and complete sequence of this protein before ordering.

Protein Length

Full Length of Mature Protein

Tag Info

N-terminal His-tagged/Tag-Free
The tag type will be determined during production process. If you have specified tag type, please tell us and we will develop the specified tag preferentially.

Storage

Store at -20°C, for extended storage, conserve at -20°C or -80°C.

Shelf Life

The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.

Notes

Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.

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Target Background

Function(From Uniprot)

Small calcium binding protein that plays important roles in several biological processes such as Ca(2+) homeostasis, chondrocyte biology and cardiomyocyte regulation. In response to an increase in intracellular Ca(2+) levels, binds calcium which triggers conformational changes. These changes allow interactions with specific target proteins and modulate their activity. Regulates a network in cardiomyocytes controlling sarcoplasmic reticulum Ca(2+) cycling and mitochondrial function through interaction with the ryanodine receptors RYR1 and RYR2, sarcoplasmic reticulum Ca(2+)-ATPase/ATP2A2 and mitochondrial F1-ATPase. Facilitates diastolic Ca(2+) dissociation and myofilament mechanics in order to improve relaxation during diastole.

Gene References into Functions

S100A1-KO exhibited increased right ventricular (RV) weight and elevated RV pressure in the absence of altered left ventricular filling pressures, increase in wall thickness of muscularized pulmonary arteries and a reduction in microvascular perfusion. PMID:25395393
S100A1 and S100B are dispensable for endochondral ossification during skeletal development. PMID:25152033
S100A1 ablationalso reduced plaque associated and increased non-plaque associated PO4-Akt and PO4-GSK3beta staining. PMID:24931125
Patients with acute myocardial infarction (MI) showed significantly increased S100A1 serum levels. Experimental MI in mice induced comparable S100A1 release. S100A1 signaling in cardiac fibroblasts occurs through endosomal TLR4/MyD88. PMID:24833748
hypoxia-induced MiR-138 is an essential mediator of EC dysfunction via its ability to target the 3'UTR of S100A1. PMID:24244340
Data suggest that the absence of S100A1 suppresses physiological AP-induced Ca(2+) release flux, resulting in impaired contractile activation and force production in skeletal muscle. PMID:20686070
Chronic absence of S100A1 results in enhanced L-type Ca2+ channel activity combined with a blunted sarcoplasmic reticulum Ca2+ release amplification. PMID:20097960
may serve as an endogenous enhancer of sarcoplasmic reticulum Ca2+ release and might therefore be of physiological relevance in the process of excitation-contraction coupling in skeletal muscle PMID:12721284
S100A1 plays an important in vivo role in the regulation of cardiac function perhaps through interacting with the ryanodine receptor PMID:12777394
study provides evidence that downregulation of S100A1 protein critically contributes to contractile dysfunction of the diseased heart, which is potentially responsible for driving the progressive downhill clinical course to postischemic heart failure PMID:16952982
S100A1 plays a role in modulating innate fear and exploration of novel stimuli. PMID:17045663
Ca(2+)-dependent interaction of S100A1 with Atpaf1 leads to an increased ATP content in cardiomyocytes. PMID:17438143
Endothelial S100A1 modulates vascular function because lack of S100A1 expression leads to decreased endothelial NO release, which contributes to impaired endothelium-dependent vascular relaxation and hypertension in SKO mice. PMID:18292599
S100A1 deficiency results in cardiac repolarization delay and alternating ventricular conduction defects in response to sympathetic activation accompanied by a significantly different transcriptional regulation. PMID:18645228
Data show that S100 appears in the inner ear later (E14) and is connected with the development of the supporting cells. PMID:19226521
Lack of S100A1 in mice confers a gender-dependent hypertensive phenotype and increased mortality after myocardial infarction. PMID:19286962
Our findings are consistent with similar activation kinetics for SR Ca(2+) channels in both WT and KO fibres, but decreased Ca(2+) release in the KO fibres possibly due to shorter SR channel open times. PMID:19651766