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Cat. No. ARG33808

ALMS1 Knockout jurkat Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Blood (peripheral blood)

  • Disease:

    Acute lymphoblastic leukemia (ALL)

The ALMS1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with disruption of the ALMS1 gene in Jurkat T lymphocyte leukemia cells. ALMS1 encodes a centrosome-associated scaffold protein that interacts with ??-actinin, myosin, IFT88, and BBSome proteins to orchestrate ciliogenesis, intracellular trafficking, and mTOR signaling. This model enables investigation of ciliopathy mechanisms, Alstr?m syndrome, and mTOR pathway regulation in T-cell leukemia. Suitable for western blotting, immunofluorescence, flow cytometry, and ciliogenesis assays.

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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

    ALMS1

    Gene Identifier

    NCBI Gene ID 7840

    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

The ALMS1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population providing a loss-of-function model for the ALMS1 gene in Jurkat T lymphocyte leukemia cells. ALMS1 encodes a centrosome-associated protein essential for primary cilia formation, intracellular trafficking, and cell cycle regulation. CRISPR/Cas9-mediated gene disruption generates a heterogeneous pool of ALMS1-knockout cells suitable for population-based functional studies.

The Jurkat cell line, derived from human acute T-cell leukemia, is an immortalized T-lymphocyte model widely used for T-cell receptor signaling, apoptosis, and cancer research. These cells express key T-cell markers and signaling pathways, and although they are non-ciliated in standard culture, ciliogenesis can be induced under specific conditions, allowing investigation of ciliary gene functions.

Mechanistically, ALMS1 localizes to centrosomes and basal bodies, scaffolding interactions with cytoskeletal and trafficking proteins. It binds ??-actinin and myosin to regulate actin dynamics, and interacts with IFT88 and BBSome proteins (e.g., BBS4) to facilitate ciliary assembly and protein transport. ALMS1 also modulates mTOR signaling by acting upstream of mTORC1, influencing Raptor and S6K. Cell cycle regulators and ciliary assembly signals control ALMS1 expression. Loss of ALMS1 disrupts these interactions, impairing ciliogenesis, mTOR signaling, and cellular stress responses.

In Jurkat cells, ALMS1 knockout enables dissection of centrosomal protein function in mTOR pathway regulation and T-cell biology. mTOR signaling governs T-cell activation, metabolism, and proliferation, and its dysregulation contributes to leukemogenesis. ALMS1 disruption in this leukemic background provides insights into how ciliopathy genes affect non-ciliated cells and offers a platform to study the interplay between centrosome-associated proteins and oncogenic signaling.

These knockout cells support applications in Alstr?m syndrome modeling, ciliopathy research, and mTOR signaling studies. Representative assays include western blotting for ALMS1 and phospho-S6K, immunofluorescence for ciliary markers, RT-qPCR, flow cytometry for cell cycle, and ciliogenesis assays. For more information, contact Ascent Research.

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