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May mediate accelerated ATP-independent bidirectional transbilayer migration of phospholipids upon binding calcium ions that results in a loss of phospholipid asymmetry in the plasma membrane. Additionally we are shipping phospholipid Scramblase 3 Antibodies (43) and many more products for this protein.
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Secreted Scr3 (show RBMS2 Proteins) was taken up by HeLa cells, suggesting that Scr3 (show RBMS2 Proteins) functions as a cell-to-cell transferable modulator carried by exosomes in a paracrine manner.
PLS3 (show PLS3 Proteins) is a downstream effector of PKC-delta (show PKCd Proteins) in the mitochondria.
PLS3 (show PLS3 Proteins) as a critical regulator of mitochondrial structure and respiration, and CL transport in apoptosis.
These findings indicate that phosphorylation of PLS3 (show PLS3 Proteins) by PKC-delta (show PKCd Proteins) induces PLS3 (show PLS3 Proteins) activation to facilitate mitochondrial targeting of tBid and apoptosis.
Identification of Alix (show PDCD6IP Proteins)-type and Non-Alix (show PDCD6IP Proteins)-type ALG-2 (show PDCD6 Proteins)-binding sites in human phospholipid scramblase 3: differential binding to an alternatively spliced isoform and amino acid-substituted mutants
TRAIL-induced activation of PKC-delta mediates regulation of the phospholipid scramblase3-induced changes in cardiolipin.
Results show that binding affinities of the peptides are in the order hPLSCR1>hPLSCR3>hPLSCR2>hPLSCR4 for Ca2 (show CA2 Proteins)+ and in the order hPLSCR1>hPLSCR2>hPLSCR3>hPLSCR4 for Mg2 (show MUC7 Proteins)+.
results suggest that Scr3 (show RBMS2 Proteins) functions as a negative regulator of adipogenesis in 3T3-L1 cells at a specific differentiation stage and that decrease in the intracellular amount of Scr3 (show RBMS2 Proteins) protein caused by reduction in Scr3 (show RBMS2 Proteins) mRNA expression
expression of PLSCR3 may be required for normal adipocyte and/or macrophage maturation or function
identified previously unrecognized lipid metabolites that suggest a novel molecular link between obesity, inflammation and the downstream consequences associated with PLSCR3-deficiency
May mediate accelerated ATP-independent bidirectional transbilayer migration of phospholipids upon binding calcium ions that results in a loss of phospholipid asymmetry in the plasma membrane. May play a central role in the initiation of fibrin clot formation, in the activation of mast cells and in the recognition of apoptotic and injured cells by the reticuloendothelial system (By similarity).
PL scramblase 3
, ca(2+)-dependent phospholipid scramblase 3
, Ca 2+ dependent phospholipid scramblase 3