mProX™ Human IKBKB Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
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Published Data
Fig.1 pS13 HTT levels are regulated by inhibitor of IKBKB and okadaic acid-sensitive phosphatases.
HEK293T cells overexpressing N571 Q55 HTT were treated with okadaic acid (OA), either in the presence or absence of IKBKB or its kinase-dead mutant IKBKB KD. When IKBKB is overexpressed in conjunction with OA therapy, Western blotting demonstrates significantly elevated pS13 HTT levels and enhanced auto-phosphorylation of IKBKB at residues S177/S181. However, IKBKB KD overexpression is not observed.
Ref: Cariulo, Cristina, et al. "IKBKB reduces huntingtin aggregation by phosphorylating serine 13 via a non-canonical IKK pathway." Life Science Alliance 6.10 (2023).
Pubmed: 37553253
DOI: 10.26508/lsa.202302006
Research Highlights
Through downregulating IKBKB, miR-200b, a transcriptional target of NF-κB, inhibits the proliferation and migration of breast cancer cells as well as NF-κB activation. This suggests that miR-200b may have use in breast cancer patients as a therapeutic target.
Wu, Hewen, et al. "A negative feedback loop between miR-200b and the nuclear factor-κB pathway via IKBKB/IKK-β in breast cancer cells." The FEBS journal 283.12 (2016): 2259-2271.
Pubmed:
26433127
DOI:
10.1111/febs.13543
This missense mutation results in very similar cellular and metabolic abnormalities in humans and mice. Precise rodent models created with CRISPR/Cas9 can provide information on pathogenesis and aid in the characterization of new syndromes resulting from de novo germline mutations.
Cardinez, Chelisa, et al. "Gain-of-function IKBKB mutation causes human combined immune deficiency." Journal of Experimental Medicine 215.11 (2018): 2715-2724.
Pubmed:
30337470
DOI:
10.1084/jem.20180639