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Cat. No. ARG39071

DNAJA2 Knockout K562 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Pleural effusion

  • Disease:

    Chronic myeloid leukemia

CRISPR/Cas9?edited polyclonal K?562 cell population with DNAJA2 gene disruption. DNAJA2 is a J?domain cochaperone that stimulates Hsp70 ATPase activity, facilitating protein folding, trafficking, and degradation. This model is derived from a CML blast crisis cell line capable of multilineage differentiation. Applications include cancer biology, protein misfolding studies, and heat shock response research. DNAJA2 interacts with HSPA1A, BAG3, and STUB1 and regulates clients like mutant p53 and Tau, making these cells ideal for drug resistance and neurodegenerative disease investigations.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    K562

    Sex of Donor

    Female

    Derived From Site

    In situ; Pleural effusion

    Gene Name

    DNAJA2

    Gene Identifier

    NCBI Gene ID 10294

    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

This product is a CRISPR/Cas9?edited polyclonal K?562 cell population carrying targeted disruption of the DNAJA2 gene, enabling loss?of?function analysis of this cochaperone. The polyclonal format preserves heterogeneous editing outcomes, avoiding clonal artifacts and supporting robust functional studies. These cells provide a ready?to?use model for investigating DNAJA2??s role in proteostasis within a hematopoietic context.

The K?562 host line, derived from a CML patient in blast crisis, is a Philadelphia chromosome?positive lymphoblast capable of spontaneous differentiation into erythrocytic, granulocytic, and monocytic lineages. Widely applied in leukemia biology and hematopoietic differentiation studies, its suspension growth and high transfectability facilitate genetic perturbation and pharmacological screening.

DNAJA2 acts as a J?domain cochaperone that stimulates Hsp70 (HSPA1A) ATP hydrolysis, stabilizing Hsp70?client complexes to drive protein folding, trafficking, and degradation. It is transcriptionally upregulated by HSF1 and ER stress sensors (IRE1, PERK, ATF6). Within the chaperone network, DNAJA2 interacts with HSPH1, BAG3, and the E3 ligases STUB1 (CHIP) and Parkin, dictating the fate of clients such as mutant p53, Tau, ???synuclein, and CFTR. This positions DNAJA2 as a key node linking stress signaling to the ubiquitin?proteasome system.

In K?562 cells, DNAJA2 disruption offers insight into how cochaperone function influences leukemic phenotypes. Because K?562 rely on Hsp70 for survival and can undergo multilineage differentiation, loss of DNAJA2 may destabilize oncogenic clients, alter differentiation trajectories, or enhance chemosensitivity. This model is therefore valuable for studying the unfolded protein response in CML and for evaluating Hsp70?targeted therapeutics.

These polyclonal knockout cells are suited for cancer biology, protein misfolding, drug resistance, and neurodegenerative disease modeling. Assays such as HSE?luciferase reporter, co?immunoprecipitation with Hsp70, Annexin V apoptosis staining, and cell cycle analysis enable comprehensive phenotypic characterization. Used alongside Western blotting, these tools facilitate dissection of DNAJA2?dependent pathways. For support, contact Ascent Research.

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