|Application ||WB, IHC-P, IF, E|
|Other Accession||NP_001035799, 105554421|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||30156 Da|
|Application Notes||SYPL2 antibody can be used for detection of SYPL2 by Western blot at 1 µg/mL. Antibody can also be used for immunohistochemistry starting at 2.5 µg/mL. For immunofluorescence start at 20 µg/mL.|
|Target/Specificity||SYPL2; At least two isoforms of SYPL2 are known to exist. SYPL2 antibody will not cross-react with SYPL1.|
|Reconstitution & Storage||SYPL2 antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.|
|Precautions||SYPL2 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Involved in communication between the T-tubular and junctional sarcoplasmic reticulum (SR) membranes.|
|Cellular Location||Membrane; Multi-pass membrane protein. Note=Triad junction, the junctional complex between the transverse tubule and the sarcoplasmic reticulum|
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Provided below are standard protocols that you may find useful for product applications.
SYPL2 Antibody: SYPL2, also known as Mitsugumin 29, was initially identified as a transmembrane protein from the triad junction in skeletal muscle that had significant homology with members of the synaptophysin family. SYPL2 is thought to participate in the excitation-contraction coupling process of skeletal muscle as SYPL2-null mice showed reduced muscle contractile force and altered triad junction structure and increased susceptibility to fatigue of the skeletal muscle. SYPL2 plays a critical role in muscle Ca2+ signaling by regulating the process of store-operated Ca2+ entry and interacts with ryanodine receptor (RyR), thereby influencing intracellular Ca2+ homeostasis through changes in the RyR/Ca2+ release function. Co-expression of SYPL2 and RyR in cultured cells leads to apoptotic cell death resulting from the depletion of Ca2+ from the intracellular stores.
Takeshima H, Simuta M, Komazaki S, et al. Mitsugumin29, a novel synaptophysin family member from the triad junction in skeletal muscle. Biochem. J.1998; 331:317-22.
Nishi M, Komazaki S, Kurebayashi Y, et al. Abnormal features in skeletal muscle from mice lacking mitsugumin29. J. Cell Biol.1999; 147:1473-80.
Nagaraj RY, Nosek CM, Brotto MA, et al. Increased susceptibility to fatigue of slow- and fast-twitch muscles from mice lacking the MG29 gene. Physiol. Genom.2000; 4:43-9.
Pan Z, Hirata D, Nagaraj RY, et al. Dysfunction of store-operated calcium channel in muscle cells lacking mg29. Nat. Cell Biol.2002; 4:379-83.
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