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Cat. No. ARG34228

HCLS1 Knockout jurkat Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Blood (peripheral blood)

  • Disease:

    Acute lymphoblastic leukemia (ALL)

HCLS1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T?lymphocyte line. The population carries targeted disruption of the HCLS1 gene, which encodes the hematopoietic adaptor protein HS1. HS1 is phosphorylated by Lyn and Syk kinases upon immune receptor activation and recruits Vav1 and Nck to promote Arp2/3?dependent actin remodeling. This knockout model enables detailed investigation of T?cell receptor signaling, leukemogenesis, and cytoskeletal?dependent processes such as migration and immune synapse formation. It is well suited for kinase inhibitor screening, functional genomics, and cell?based assays to dissect HS1?mediated pathways.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    Jurkat

    Cell Type

    T cell line

    Sex of Donor

    Male

    Age

    14 years

    Derived From Site

    In situ; Peripheral blood

    Gene Name

    HCLS1

    Gene Identifier

    NCBI Gene ID 3059

    Growth Mode

    Suspension

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    RPMI 1640

    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

HCLS1 Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in which the HCLS1 gene has been disrupted using targeted Cas9 nucleases. The polyclonal format consists of a heterogeneous pool of edited cells carrying diverse loss-of-function alleles at the HCLS1 locus, providing a robust model for studying gene function without clonal artifacts. This product is designed for researchers investigating T?cell receptor (TCR) signaling, cytoskeletal dynamics, and malignant transformation.

The host Jurkat cell line is an immortalized human T?lymphocyte line originally derived from the peripheral blood of a 14?year?old boy with acute T?cell leukemia. Jurkat cells are widely used as a model system for TCR?mediated signal transduction, leukemia biology, and T?cell activation owing to their well?characterized signaling machinery and ease of genetic manipulation. Their leukemic origin also makes them particularly relevant for studying oncogenic signaling pathways.

HCLS1 encodes the hematopoietic lineage cell?specific protein HS1, a key adaptor protein that links immune receptor engagement to cytoskeletal reorganization. Upon TCR stimulation, HS1 is phosphorylated by upstream kinases Lyn and Syk, enabling recruitment of the guanine nucleotide exchange factor Vav1 and the adaptor Nck. This complex activates the Arp2/3 complex, which drives actin branching and polymerization, thereby facilitating immune synapse formation, cell spreading, and migration. HS1 also interacts with HAX?1 and participates in chemokine and B?cell receptor pathways, making it a central node in immune signaling.

In the Jurkat T?cell context, disruption of HCLS1 abrogates HS1?dependent actin remodeling and impairs downstream functional responses, including TCR?induced activation, adhesion, and migratory capacity. This knockout model enables dissection of the specific contribution of HS1 to leukemic T?cell signaling and may reveal vulnerabilities exploitable for therapeutic intervention. The polyclonal nature of the population mirrors the heterogeneity observed in tumor samples, enhancing translational relevance.

Typical applications include mechanistic studies of immune signaling, anti?leukemic drug screening, kinase inhibitor profiling, and functional genomics. Representative assays with these cells include western blotting to assess HS1 phosphorylation and downstream effector activation, flow cytometry for TCR?induced surface markers, transwell migration and invasion assays, co?immunoprecipitation to map HS1 interaction networks, and confocal microscopy to visualize actin cytoskeleton reorganization. For technical inquiries and ordering information, please contact Ascent Research.

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