PLG Easy KO Kit

Name: PLG Easy KO Kit
SKU: CC-1094
Availability: InStock

For research use only. Not intended for any clinical use.

Cat. No. : CC-1094

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Product Information

Gene Information

Cat. No.	CC-1094
Description	A complete kit for efficient gene knockout in mammalian cells, combining chemically synthesized sgRNAs with Cas9 RNPs to induce targeted DNA cleavage and generate frameshift mutations or deletions. All essential reagents for transfection and knockout validation are included for rapid, high-efficiency gene disruption.
Gene Abbr	PLG
Species	Human
Ensembl ID	ENSG00000122194
NCBIGene ID	5340
Uni Prot ID	P00747
Features	All-in-One workflow from gene editing to knockout validation for users with no prior experience. Pre-validated sgRNAs and primers for rapid setup. Streamlined experiment handling. CRISPR RNP method ensures precise and efficient gene knockout.
Applications	This kit enables in vitro gene knockout in human-derived cells using chemically synthesized sgRNAs and Cas9-gRNA RNP complexes. Transfected RNPs cleave early exons of the target gene, inducing deletions or frameshift mutations for efficient and rapid knockout.
Reactions	5–10 reactions per target gene
Kit Components	2–3 chemically synthesized sgRNAs (200pmol each) 3 PCR/Sequencing primers (500pmol each) LM cell lysate (500µL) Cas9 protein (12µg) LM RNP transfection reagent (50µL)
Storage	Store at -80°C for up to 1 year or at -20°C for up to 6 months. Avoid repeated freeze-thaw cycles.

Target Gene

PLG

Background

The plasminogen protein encoded by this gene is a serine protease that circulates in blood plasma as an inactive zymogen and is converted to the active protease, plasmin, by several plasminogen activators such as tissue plasminogen activator (tPA), urokinase plasminogen activator (uPA), kallikrein, and factor XII (Hageman factor). The conversion of plasminogen to plasmin involves the cleavage of the peptide bond between Arg-561 and Val-562. Plasmin cleavage also releases the angiostatin protein which inhibits angiogenesis. Plasmin degrades many blood plasma proteins, including fibrin-containing blood clots. As a serine protease, plasmin cleaves many products in addition to fibrin such as fibronectin, thrombospondin, laminin, and von Willebrand factor. Plasmin is inactivated by proteins such as alpha-2-macroglobulin and alpha-2-antiplasmin in addition to inhibitors of the various plasminogen activators. Plasminogen also interacts with plasminogen receptors which results in the retention of plasmin on cell surfaces and in plasmin-induced cell signaling. The localization of plasminogen on cell surfaces plays a role in the degradation of extracellular matrices, cell migration, inflamation, wound healing, oncogenesis, metastasis, myogenesis, muscle regeneration, neurite outgrowth, and fibrinolysis. This protein may also play a role in acute respiratory distress syndrome (ARDS) which, in part, is caused by enhanced clot formation and the suppression of fibrinolysis. Compared to other mammals, the cluster of plasminogen-like genes to which this gene belongs has been rearranged in catarrhine primates. [provided by RefSeq, May 2020]

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