Recombinant Mouse NFKBIZ Protein

• Cat.No.: NFKBIZ-10629M
• Product Overview: Recombinant Mouse NFKBIZ full length or partial length protein was expressed.

Specification

• Species: Mouse
• Source: Mammalian Cells
• Tag: His
• Form: Liquid or lyophilized powder
• Endotoxin: < 1.0 EU per μg of the protein as determined by the LAL method.
• Purity: >80%
• Notes: This item requires custom production and lead time is between 5-9 weeks. We can custom produce according to your specifications.
• Storage: Store it at +4 ºC for short term. For long term storage, store it at -20 ºC～-80 ºC.
• Storage Buffer: PBS buffer

Gene Information

• Gene Name: Nfkbiz nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, zeta [ Mus musculus ]
• Official Symbol: NFKBIZ
• Gene ID: 80859
• mRNA Refseq: NM_001159394.1
• Protein Refseq: NP_001152866.1
• UniProt ID: Q9EST8

Case Study

Case 1: Guo D, et al. Cell Mol Life Sci. 2024

Hepatocellular carcinoma (HCC) is a prevalent and deadly cancer, with NFKBIZ, a nuclear factor kappa B inhibitory family member, potentially influencing its progression. The comprehensive experiments, ranging from clinical to cellular analyses, showed that reduced NFKBIZ expression in HCC tissues correlated with a poorer patient prognosis and advanced disease stage. In vitro assays demonstrated that increased NFKBIZ levels were linked to decreased HCC cell proliferation, invasion, and migration. In vivo studies confirmed that NFKBIZ overexpression suppressed tumor growth and metastasis. Further analysis showed NFKBIZ's regulatory effect on HCC cell growth and migration through the NFκB signaling pathway. Lastly, TRIM16 interacts with NFKBIZ, promoting its ubiquitination and degradation, which may reduce HCC cell apoptosis and contribute to sorafenib resistance.

Fig1. Western blot was employed to detect the expression of NFKBIZ protein.

Fig2. The Co-IP result was presented via Western blot, showing the interactions between TRIM16 and NFKBIZ.

Case 2: Poveda J, et al. Biochim Biophys Acta. 2016

Acute kidney injury (AKI) is marked by renal dysfunction, cell death, and inflammation, with NF-κB being a central regulator of cell survival and inflammation. This study investigated NF-κB-related gene expression in AKI triggered by folic acid toxicity. NFκBiz, an IκB family member, was highly upregulated at the mRNA level but downregulated at the protein level in AKI. This pattern was also seen in AKI from other causes, such as cisplatin or ureteral obstruction. In cultured tubular cells, NFκBiz was induced by inflammatory stimuli but had a minor response to TWEAK. Knocking down NFκBiz increased chemokine production, affected Klotho regulation, and made cells more resistant to apoptosis, suggesting its role in AKI pathophysiology.

Fig1. NFκBiz is expressed by kidney tubules.

Fig2. Representative Western blot and quantification of NFκBiz in renal tissue lysates at day 5.

Application

Recombinant Mouse NFKBIZ Protein is an important immunomodulatory protein belonging to the nuclear factor κB (NFκB) suppressor protein family. By binding to NF-κB in the nucleus, it inhibits the activation of the NF-κB signaling pathway, thereby affecting the expression of downstream genes. NFKBIZ plays a role in a variety of biological processes, including immune response, inflammatory response, and tumor initiation and development.

In practical applications, research on NFKBIZ has focused on its effect on tumor development. For example, in hepatocellular carcinoma (HCC), NFKBIZ expression levels are strongly associated with patient prognosis. We found that NFKBIZ can inhibit the proliferation and metastasis of HCC cells by regulating the NFκB signaling pathway and is associated with the epithelial-mesenchymal transformation (EMT) process of tumors. In addition, overexpression of NFKBIZ can enhance the apoptosis rate of HCC cells, which may contribute to increased sensitivity to sorafenib therapy.

In the field of drug development, NFKBIZ is considered a potential therapeutic target, especially in improving the response of HCC to sorafenib therapy. By enhancing the expression of NFKBIZ or inhibiting its ubiquitination degradation, it may be helpful to improve the therapeutic effect of HCC. In addition, NFKBIZ's role in other types of tumors, such as bladder cancer, rectal cancer, and diffuse large B-cell lymphoma (DLBCL), has also been extensively studied, indicating its broad potential in tumor therapy.

Fig1. Signaling pathways involved in IκBζ induction. (Yanpeng Feng, 2023)