Camk2d (NM_001025439) Mouse Tagged ORF Clone Lentiviral Particle
CAT#: MR222605L4V
- LentiORF®
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Lenti ORF particles, Camk2d (GFP-tagged) - Mouse calcium/calmodulin-dependent protein kinase II, delta (Camk2d), transcript variant 1, 200ul, >10^7 TU/mL
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CNY 10,830.00
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Specifications
Product Data | |
Product Name | Camk2d (NM_001025439) Mouse Tagged ORF Clone Lentiviral Particle |
Synonyms | 2810011D23Rik; 8030469K03Rik; CaMK II; [d]-CaMKII |
Vector | pLenti-C-mGFP-P2A-Puro |
ACCN | NM_001025439 |
ORF Size | 1536 bp |
Sequence Data |
The ORF insert of this clone is exactly the same as(MR222605).
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OTI Disclaimer | The molecular sequence of this clone aligns with the gene accession number as a point of reference only. However, individual transcript sequences of the same gene can differ through naturally occurring variations (e.g. polymorphisms), each with its own valid existence. This clone is substantially in agreement with the reference, but a complete review of all prevailing variants is recommended prior to use. More info |
OTI Annotation | This clone was engineered to express the complete ORF with an expression tag. Expression varies depending on the nature of the gene. |
Reference Data | |
RefSeq | NM_001025439.1 |
RefSeq Size | 4299 bp |
RefSeq ORF | 1539 bp |
Locus ID | 108058 |
Gene Summary | Calcium/calmodulin-dependent protein kinase involved in the regulation of Ca(2+) homeostatis and excitation-contraction coupling (ECC) in heart by targeting ion channels, transporters and accessory proteins involved in Ca(2+) influx into the myocyte, Ca(2+) release from the sarcoplasmic reticulum (SR), SR Ca(2+) uptake and Na(+) and K(+) channel transport. Targets also transcription factors and signaling molecules to regulate heart function. In its activated form, is involved in the pathogenesis of dilated cardiomyopathy and heart failure. Contributes to cardiac decompensation and heart failure by regulating SR Ca(2+) release via direct phosphorylation of RYR2 Ca(2+) channel on 'Ser-2808'. In the nucleus, phosphorylates the MEF2 repressor HDAC4, promoting its nuclear export and binding to 14-3-3 protein, and expression of MEF2 and genes involved in the hypertrophic program. Is essential for left ventricular remodeling responses to myocardial infarction. In pathological myocardial remodeling acts downstream of the beta adrenergic receptor signaling cascade to regulate key proteins involved in ECC. Regulates Ca(2+) influx to myocytes by binding and phosphorylating the L-type Ca(2+) channel subunit beta-2 CACNB2. In addition to Ca(2+) channels, can target and regulate the cardiac sarcolemmal Na(+) channel Nav1.5/SCN5A and the K+ channel Kv4.3/KCND3, which contribute to arrhythmogenesis in heart failure. Phosphorylates phospholamban (PLN/PLB), an endogenous inhibitor of SERCA2A/ATP2A2, contributing to the enhancement of SR Ca(2+) uptake that may be important in frequency-dependent acceleration of relaxation (FDAR) and maintenance of contractile function during acidosis. May participate in the modulation of skeletal muscle function in response to exercise, by regulating SR Ca(2+) transport through phosphorylation of PLN/PLB and triadin, a ryanodine receptor-coupling factor.[UniProtKB/Swiss-Prot Function] |
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