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Involved in the modulation of the mitochondrial apoptotic pathway by ensuring the accumulation of cardiolipin (CL) in mitochondrial membranes. In vitro, the TRIAP1:PRELID1 complex mediates the transfer of phosphatidic acid (PA) between liposomes and probably functions as a PA transporter across the mitochondrion intermembrane space to provide PA for CL synthesis in the inner membrane. Regulates the mitochondrial apoptotic pathway in primary Th cells. Regulates Th cell differentiation by down-regulating STAT6 thereby reducing IL-4-induced Th2 cell number. May be important for the development of vital and immunocompetent organs.
Gene References into Functions
This study suggests that the regulation of PRELID1 expression, by alternative polyadenylation and other mechanisms, plays a role in mitochondrial ROS signaling and represents a novel prognostic factor and therapeutic target in cancer PMID: 28912168
PRELI plays an important role in the suppression of apoptosis in HepG2 cells in response to oxidative stress. PMID: 26275693
Loss of TRIAP1 or PRELI impairs the accumulation of Cardiolipin, facilitates the release of cytochrome c, and renders cells vulnerable to apoptosis upon intrinsic and extrinsic stimulation. PMID: 23931759
PRELI is a vital LEA B cell protein with failsafe genetics PMID: 22666421
PRELI interacts with OPA1 to maintain mitochondria structures intact, sustain balanced ion(-)/proton(+) gradients, promote oxidative phosphorylation reactions, regulate pro- and antiapoptotic protein traffic and enable cell responses to induced death. PMID: 21364629
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Subcellular Location
Mitochondrion. Mitochondrion intermembrane space.
Tissue Specificity
Highly expressed in fetal liver; less expressed in fetal brain, lung, and kidney. At the adult stage, expression is drastically reduced in the liver but highly expressed in the spleen, brain, lung, lymph nodes and peripheral blood leukocytes.