PCSK9 Blocking Peptide for STJ501875 is synthetically produced from the 30-60 sequence and is suitable for use in western blot applications.
Applications
Immunodepletion/Immunocompetition
Note
STRICTLY FOR FURTHER SCIENTIFIC RESEARCH USE ONLY (RUO). MUST NOT TO BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS.
Product Properties
Formulation
Liquid form at 2.5mg/ml concentration in PBS. Up to 5% DMSO can be added. Orders with >1mg can be supplied in lyophilized powder form, or in buffer of choice.
Storage Instruction
Store at-20°C for long term storage. Avoid freeze-thaw cycles.
Cleavage by furin and PCSK5 generates a truncated inactive protein that is unable to induce LDLR degradation. Undergoes autocatalytic cleavage in the endoplasmic reticulum to release the propeptide from the N-terminus and the cleavage of the propeptide is strictly required for its maturation and activation. The cleaved propeptide however remains associated with the catalytic domain through non-covalent interactions, preventing potential substrates from accessing its active site. As a result, it is secreted from cells as a propeptide-containing, enzymatically inactive protein. Phosphorylation protects the propeptide against proteolysis.
Function
Crucial player in the regulation of plasma cholesterol homeostasis. Binds to low-density lipid receptor family members: low density lipoprotein receptor (LDLR), very low density lipoprotein receptor (VLDLR), apolipoprotein E receptor (LRP1/APOER) and apolipoprotein receptor 2 (LRP8/APOER2), and promotes their degradation in intracellular acidic compartments. Acts via a non-proteolytic mechanism to enhance the degradation of the hepatic LDLR through a clathrin LDLRAP1/ARH-mediated pathway. May prevent the recycling of LDLR from endosomes to the cell surface or direct it to lysosomes for degradation. Can induce ubiquitination of LDLR leading to its subsequent degradation. Inhibits intracellular degradation of APOB via the autophagosome/lysosome pathway in a LDLR-independent manner. Involved in the disposal of non-acetylated intermediates of BACE1 in the early secretory pathway. Inhibits epithelial Na(+) channel (ENaC)-mediated Na(+) absorption by reducing ENaC surface expression primarily by increasing its proteasomal degradation. Regulates neuronal apoptosis via modulation of LRP8/APOER2 levels and related anti-apoptotic signaling pathways.
CytoplasmSecretedEndosomeLysosomeCell SurfaceEndoplasmic ReticulumGolgi ApparatusAutocatalytic Cleavage Is Required To Transport It From The Endoplasmic Reticulum To The Golgi Apparatus And For The Secretion Of The Mature ProteinLocalizes To The Endoplasmic Reticulum In The Absence Of Ldlr And Co-Localizes To The Cell Surface And To The Endosomes/Lysosomes In The Presence Of LdlrThe Sorting To The Cell Surface And Endosomes Is Required In Order To Fully Promote Ldlr Degradation
Alternative Peptide Names
Proprotein Convertase Subtilisin/Kexin Type 9 proteinNeural Apoptosis-Regulated Convertase 1 proteinNarc-1 proteinProprotein Convertase 9 proteinPc9 proteinSubtilisin/Kexin-Like Protease Pc9 proteinPcsk9 proteinNarc1 protein
