In Stock Cell Lines
The Rab27a Knockout LLC Cell Line is a CRISPR/Cas9-edited knockout cell line derived from mouse LLC lung carcinoma epithelial cells. This loss-of-function model disrupts the Rab27a gene, which encodes a small GTPase regulating secretory vesicle docking and exocytosis. Rab27a is activated by Rab3GEP/MADD and calcium signaling and recruits effectors including SYTL2/Slp2-a and melanophilin to mediate melanosome transport, lytic granule secretion, and exosome release. The syngeneic LLC host line is a standard model for metastatic lung carcinoma and drug testing. This knockout enables functional studies of Rab27a in exosome biogenesis, tumor metastasis, and immune degranulation, with relevance to cancer biology, immunology, and Griscelli syndrome type 2.
MPP7 Knockout HT29 Polyclonal Cells
Cat. No. ARG14309
PDP1 Knockout Hela Polyclonal Cells
Cat. No. ARG8052
APOBEC3A Knockout A549 Polyclonal Cells
Cat. No. ARG35602
CAB39L Knockout A549 Polyclonal Cells
Cat. No. ARG41707
HPS6 Knockout HAP1 Polyclonal Cells
Cat. No. ARG27575
CANX Knockout huh-7 Polyclonal Cells
Cat. No. ARG28178
The Rab27a Knockout LLC Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the murine LLC (Lewis lung carcinoma) cell line. This targeted disruption of the Rab27a gene generates a loss-of-function model to elucidate the roles of this small GTPase in intracellular trafficking and exocytosis. The knockout cell pool offers a genetically uniform background for interrogating Rab27a-dependent pathways without clonal selection artifacts.
LLC cells originate from a spontaneous lung carcinoma in the C57BL/6 mouse strain, to which they are syngeneic, enabling straightforward allograft studies. These epithelial cells are highly metastatic, predominantly to the lungs, and serve as a cornerstone model for tumor biology, angiogenesis, and metastasis research. They are routinely employed in preclinical testing of anticancer agents and in mechanistic studies of tumor?Chost interactions.
Rab27a is a Rab family GTPase that shuttles between an inactive GDP-bound and active GTP-bound state. Activation by the guanine nucleotide exchange factor Rab3GEP/MADD, triggered by calcium signaling, promotes GTP-bound Rab27a to recruit effector proteins including SYTL2/Slp2-a, melanophilin, and Munc13-4. These effectors tether secretory vesicles to the plasma membrane, facilitating exocytosis of melanosomes, lytic granules, and exosomes. Rab27a also interacts with Myosin Va and the exocyst complex to coordinate vesicle transport and fusion, thus regulating pigmentation, immune cell degranulation, and hormone release.
In the LLC metastatic lung carcinoma context, Rab27a is pivotal for exosome-mediated communication that shapes the tumor microenvironment. Loss of Rab27a impairs secretion of tumor-derived exosomes loaded with pro-invasive and immunosuppressive cargo, thereby dampening metastatic niche formation and drug resistance. This knockout cell line is therefore a critical tool to dissect how Rab27a-driven exocytosis contributes to cancer progression and to evaluate the intrinsic role of Rab27a in tumor cell migration and invasion.
Research applications span exosome biogenesis and function, metastasis mechanisms, and immune cell degranulation studies in syngeneic models. Key assays include Western blotting for Rab27a confirmation, RT-qPCR for transcript analysis, immunofluorescence localization, exosome isolation with nanoparticle tracking, Boyden chamber migration/invasion assays, and in vivo metastasis modeling. Co-immunoprecipitation can map effector interactions, and flow cytometry or ELISA-based secretion assays quantify granule or cytokine release. For further details, please contact Ascent Research.
