Targeted disruption of TAK1 in HEK293 cells via CRISPR/Cas 9: A tool for functional dissection of inflammatory and autophagic signaling

Targeted disruption of TAK1 in HEK293 cells via CRISPR/Cas 9: A tool for functional dissection of inflammatory and autophagic signaling | Zenodo Skip to main Communities My dashboard Log in Sign up Zenodo is currently experiencing slowness and intermittent outages due to heavy automated traffic from bots and AI crawlers. We are aware of the problem, and our team is focused on stabilizing the service. Thank you for your patience. Published May 1, 2026 | Version v1 Journal article Open Targeted disruption of TAK1 in HEK293 cells via CRISPR/Cas 9: A tool for functional dissection of inflammatory and autophagic signaling Authors/Creators Tawseeq Abdullah Waseem Rashid Asiya Batool Mohammad Afzal Zargar Khurshid Iqbal Andrabi Description Abstract : Transforming growth factor-β activated kinase1 (TAK1) is a serine threonine kinase stimulated by TGF- β, in addition to other stimuli including inflammatory cytokines, microbial products and environmental stress. TAK1 regulates multiple cellular events notably developmental processes, differentiation, autophagy, apoptosis and cell survival through extensive cross-talk with crucial signalling pathways like, MAP kinases, IKK and JNK. On one hand it engages with energy sensor mechanisms via AMPK and on the other with growth regulation processes dominated by mTOR signaling. By creating a stable TAK1 knockout cell line, we can dissect how loss of TAK1 affects mTORC1 activation, autophagy induction, and cell survival under conditions of nutrient restriction or metabolic stress, thereby clarifying whether TAK1 functions as a pro‑survival, pro‑death, or context‑dependent modulator in hyperproliferative and aging‑like states. For this, three sgRNAs were designed for TAK1 gene. The sgRNA1 and sgRNA2 with the higher activity were respectively used to construct pSpCas9(BB)-2A-Puro-sgRNA1 and pSpCas9(BB)-2A-Puro-sgRNA2. The knockout plasmid vectors were transfected into HEK-293 cells. Through drug screening, the TAK1 gene-knockout HEK293 (TAK1 -/- ) cell lines was obtained which was subsequently confirmed with Western blotting and sequencing. This isogenic CRISPR‑derived knockout line will also provide a clean genetic background for rescue experiments and pharmacological studies, improving mechanistic rigour and enabling us to identify TAK1‑dependent nodes that could be targeted for therapeutic intervention in cancer or age‑related pathologies. Keywords: CRISPR/Cas, TAK1, mTOR, Puromycin. Title: Targeted disruption of TAK1 in HEK293 cells via CRISPR/Cas 9: A tool for functional dissection of inflammatory and autophagic signaling Author: Tawseeq Abdullah, Waseem Rashid, Asiya Batool, Mohammad Afzal Zargar, Khurshid Iqbal Andrabi International Journal of Life Sciences Research ISSN 2348-313X (Print), ISSN 2348-3148 (online) Vol. 14, Issue 2, April 2026 - June 2026 Page No: 5-11 Research Publish Journals Website: www.researchpublish.com Published Date: 01-May-2026 DOI: https://doi.org/10.5281/zenodo.19952933 Paper Download Link (Source) https://www.researchpublish.com/papers/targeted-disruption-of-tak1-in-hek293-cells-via-crisprcas-9-a-tool-for-functional-dissection-of-inflammatory-and-autophagic-signaling Files Targeted disruption of TAK1 in HEK293-01052026-2.pdf Files (1.3 MB) Name Size Download all Targeted disruption of TAK1 in HEK293-01052026-2.pdf md5:863b1f3e4e2a7417f371992d83019e76 1.3 MB Preview Download Additional details Identifiers ISSN 2348-313X EISSN 2348-3148 URL https://www.researchpublish.com/papers/targeted-disruption-of-tak1-in-hek293-cells-via-crisprcas-9-a-tool-for-functional-dissection-of-inflammatory-and-autophagic-signaling 27 Views 10 Downloads Show more details All versions This version Views Total views 27 27 Downloads Total downloads 10 10 Data volume Total data volume 12.6 MB 12.6 MB More info on how stats are collected.... Versions External resources Indexed in OpenAIRE Communities Keywords and subjects Keywords CRISPR/Cas TAK1 mTOR Puromycin Details DOI DOI Badge DOI 10.5281/zenodo.19952933 Markdown [](https://doi.org/10.5281/zenodo.19952933) reStructuredText .. image:: https://zenodo.org/badge/DOI/10.5281/zenodo.19952933.svg :target: https://doi.org/10.5281/zenodo.19952933 HTML <a href="https://doi.org/10.5281/zenodo.19952933"><img src="https://zenodo.org/badge/DOI/10.5281/zenodo.19952933.svg" alt="DOI"></a> Image URL https://zenodo.org/badge/DOI/10.5281/zenodo.19952933.svg Target URL https://doi.org/10.5281/zenodo.19952933 Resource type Journal article Publisher Research Publish Journals (www.researchpublish.com) Published in International Journal of Life Sciences Research, 14(2), 5-11, ISSN: 2348-313X, 2026. Languages English Rights License Creative Commons Attribution 4.0 International The Creative Commons Attribution license allows re-distribution and re-use of a licensed work on the condition that the creator is appropriately credited. Read more Citation Export Technical metadata Created May 5, 2026 Modified May 5, 2026 Jump up About About Policies Infrastructure Principles Projects Roadmap Contact Blog Blog Support Help FAQ Developers REST API OAI-PMH Contribute GitHub Donate Funded by Powered by CERN Data Centre & InvenioRDM Status Privacy policy Cookie policy Terms of Use This site uses cookies. Find out more on how we use cookies Accept all cookies Accept only essential cookies

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