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Home / Products / Genome-edited Cells / Knockout Cell Lines / ABLIM1 Knockout huh-7 Polyclonal Cells

Cat. No. ARG27757

ABLIM1 Knockout huh-7 Polyclonal Cells

Product Type:
Polyclonal Cell Population
Species:
Homo sapiens (Human)
Tissue Source:
Liver
Disease:
Hepatocellular carcinoma

Datasheet

ABLIM1 Knockout Huh-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population with targeted disruption of the ABLIM1 gene in the Huh-7 human hepatocellular carcinoma line. ABLIM1 is an actin-binding LIM domain protein that mediates cytoskeletal organization, focal adhesion dynamics, and integrin signaling, interacting with vinculin, talin, and actin filaments to regulate cell adhesion and migration. This knockout model enables investigation of actin remodeling, Rho GTPase signaling, and metastatic behavior in liver cancer, supporting functional assays such as Transwell migration, immunofluorescence, and phospho-signaling analyses. It provides a robust tool for studying ABLIM1-dependent pathways in hepatocellular carcinoma progression.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice

Disclaimer:

For Research Use Only

Characteristics

Host Cell

Huh-7

Sex of Donor

Male

Age

57 years

Gene Name

ABLIM1

Gene Identifier

NCBI Gene ID 3983

Morphology

Epithelial-like

Growth Mode

Adherent

Storage

Liquid nitrogen (LN2)
Culture Conditions

Growth medium

DMEM

Supplement(s)

10% Fetal Bovine Serum, 1% Penicillin-Streptomycin Solution

Temperature

37°C

Atmosphere

5% CO₂
Quality Control

Sterility testing

The bacterial, yeast, and fungi are not detected in these cells by daily monitor.

Mycoplasma testing

Negative for mycoplasma through PCR analysis
Disclaimer

Intended Use

This product is intended for laboratory in vitro use only. lt is not intended for diagnostic, therapeutic, or clinical applications.

Disclaimer

Ascent Research endeavors to provide accurate and up-to-date product information. However, no warranties or representations are made regarding its completeness or reliability. References to scientific literature and patents are for informational purposes only, and the customer assumes sole responsibility for verifying their accuracy.

By accepting this product, the customer acknowledges and agrees to assume all risks associated with its receipt, handling, storage, disposal, and use, including compliance with all applicable safety and environmental regulations and precautions. Relevant laws, regulations, and ethical guidelines must be followed in conducting any research, modifications, or derivatives derived from this product.

This product is provided "AS IS", and except as expressly stated herein, Ascent Research disclaims all other warranties, express or implied. Under no circumstances shall Ascent Research, its affiliates, or representatives be liable for indirect, incidental, consequential, or punitive damages arising from the use of this material. While Ascent Research employs rigorous quality control measures, we shall not be held responsible for damages resulting from misidentification or misinterpretation of the provided materials.

Description

The ABLIM1 Knockout Huh-7 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal cell population engineered for targeted disruption of the ABLIM1 gene in the Huh-7 human hepatocellular carcinoma line. This reagent provides a loss-of-function model to investigate the role of the actin-binding LIM protein 1 in liver cancer biology, avoiding clonal selection artifacts through polyclonal representation.

The parental Huh-7 cell line, established in 1982 from a well-differentiated hepatocellular carcinoma of a 57-year-old Japanese male, exhibits adherent epithelial morphology and is widely employed for studying hepatocarcinogenesis, hepatitis C virus replication, and hepatic drug metabolism. Its robust growth and well-characterized signaling networks offer a reliable platform for knockout studies.

ABLIM1 encodes an actin-binding protein that integrates LIM and villin-like domains to couple filamentous actin with focal adhesion complexes. It operates downstream of RhoA and TGF-beta signaling, interacts with vinculin, talin, and alpha-actinin, and modulates actin polymerization and focal adhesion kinase (FAK) activity. Through these interactions, ABLIM1 influences cadherin-mediated adhesion and matrix metalloproteinase expression, placing it at the nexus of cytoskeletal remodeling and integrin-mediated mechanotransduction.

In the Huh-7 hepatocellular carcinoma background, disruption of ABLIM1 is predicted to destabilize actin cytoskeletal architecture and compromise focal adhesion assembly, thereby attenuating cell adhesion and migratory capacity. This perturbation likely alters Rho GTPase-driven signaling and downstream FAK-paxillin cascades, diminishing invasive behavior and offering a system to dissect pathways governing liver cancer metastasis.

Researchers can employ these polyclonal knockout cells to explore actin cytoskeletal reorganization and focal adhesion dynamics in hepatocellular carcinoma, utilizing immunofluorescence for F-actin and vinculin, Transwell migration and invasion assays, and Rho activity pulldown analyses. The model supports phospho-signaling profiling of FAK and paxillin, wound healing studies, and adhesion assays to clarify ABLIM1??s role in metastatic progression. For further technical information or ordering, please contact Ascent Research.