|Application ||WB, E|
|Calculated MW||31195 Da|
|Antigen Region||51-79 aa|
|Other Names||Pleckstrin homology domain-containing family F member 1, PH domain-containing family F member 1, Lysosome-associated apoptosis-inducing protein containing PH and FYVE domains, Apoptosis-inducing protein, PH and FYVE domain-containing protein 1, Phafin-1, Zinc finger FYVE domain-containing protein 15, PLEKHF1, APPD, LAPF, ZFYVE15|
|Target/Specificity||This PLEKHF1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 51-79 amino acids from the N-terminal region of human PLEKHF1.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||PLEKHF1 Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Synonyms||APPD, LAPF, ZFYVE15|
|Function||May induce apoptosis through the lysosomal-mitochondrial pathway. Translocates to the lysosome initiating the permeabilization of lysosomal membrane (LMP) and resulting in the release of CTSD and CTSL to the cytoplasm. Triggers the caspase- independent apoptosis by altering mitochondrial membrane permeabilization (MMP) resulting in the release of PDCD8.|
|Cellular Location||Nucleus. Cytoplasm, perinuclear region Lysosome. Note=Translocates to lysosome during apoptosis|
|Tissue Location||Highly expressed in heart and skeletal muscle. Weakly expressed in brain, thymus, spleen, kidney, liver, small intestine, placenta and lung.|
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Provided below are standard protocols that you may find useful for product applications.
PLEKHF1 may induce apoptosis through the lysosomal-mitochondrial pathway. Translocates to the lysosome initiating the permeabilization of lysosomal membrane (LMP) and resulting in the release of CTSD and CTSL to the cytoplasm. Triggers the caspase-independent apoptosis by altering mitochondrial membrane permeabilization (MMP) resulting in the release of PDCD8.
Chen, W., et al. J. Biol. Chem. 280(49):40985-40995(2005)
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