In Stock Cell Lines
The Septin5 Knockout AML12 Cell Line provides a CRISPR/Cas9-edited loss?of?function model in the non?transformed AML12 mouse hepatocyte line, enabling investigation of Septin5 roles in hepatic vesicle trafficking and secretion. This gene encodes a septin GTPase that interacts with syntaxin?1A, VAMP2, and dynamin to regulate SNARE?complex?dependent exocytosis downstream of insulin and cAMP pathways. Applications include studying septin?mediated exocytosis of albumin and transferrin, modeling secretion defects, and screening modulators via immunofluorescence, ELISA?based assays, and vesicle dynamics measurements. For more details, contact Ascent Research.
FAM114A1 Knockout NCI-H1299 Polyclonal Cells
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FGF18 Knockout MCF7 Polyclonal Cells
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MPV17 Knockout Raji Polyclonal Cells
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Saos-2
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The Septin5 Knockout AML12 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the AML12 murine hepatocyte line, offering a targeted loss-of-function model for Septin5 (SEPT5). This product enables researchers to investigate the cellular consequences of Septin5 disruption in a non?transformed hepatic cell background, without the need for transient knockdown approaches. The knockout cell line is provided in a ready?to?use format, facilitating the study of septin?dependent processes in liver parenchymal cells.
The AML12 parental cell line was established from the hepatocytes of a CD1 mouse and retains key features of primary hepatocytes, including the capacity for albumin and transferrin synthesis and secretion. As a non?transformed cell line, AML12 maintains normal growth control and hepatocyte?specific functions, making it a physiologically relevant model for investigating hepatic secretory pathways, metabolism, and cell division. Its adherent growth characteristics and stable phenotype support both short?term mechanistic studies and longer?term loss?of?function assays.
Septin5 encodes a filamentous GTPase that assembles into hetero?oligomeric complexes predominantly with SEPT4 and SEPT7, thereby regulating cytoskeletal organization and membrane dynamics. In the context of membrane traffic, Septin5 functions downstream of insulin signaling and cAMP?dependent pathways to modulate SNARE?mediated exocytosis. At the molecular level, Septin5 directly interacts with syntaxin?1A, syntaxin?4, VAMP2, and dynamin, and it influences the assembly and stability of the core SNARE complex composed of syntaxin?1A, VAMP2, SNAP?25, and NSF. Through these interactions, Septin5 governs vesicle docking and fusion at the plasma membrane, impacting the secretion of hepatic proteins.
Knockout of Septin5 in AML12 hepatocytes is predicted to impair the exocytic release of major serum proteins such as albumin and transferrin, while also potentially affecting cytokinesis due to the role of septins in the contractile ring. This model is therefore valuable for dissecting the contribution of septin filaments to hepatocyte secretory capacity and cell division fidelity. Since aberrant septin expression has been implicated in neurological disorders and platelet?related diseases, the AML12 knockout line also provides a platform for evaluating hepatocyte?autonomous consequences of Septin5 loss that may be relevant to conditions like Parkinson disease and Bernard?Soulier syndrome, albeit in a hepatic context.
Typical experimental applications include monitoring labeled vesicle dynamics using FM dyes, quantifying secreted proteins by ELISA?based exocytosis assays, and assessing proliferation rates. The line is also suitable for immunofluorescence staining to examine septin localization and for screening chemical modulators that could restore or bypass the secretory defects. In addition, researchers can perform western blotting to measure intracellular and secreted albumin and transferrin levels, enabling functional dissection of septin?dependent trafficking. For detailed product specifications and availability, please contact Ascent Research.
