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NF-KB

BOC Sciences provides various cytotoxin that act as payloads to conjugate with antibodies and form ADCs. The Nuclear Factor Kappa-B (NF-KB) family consists of transcription factors that play complex and essential roles in regulating immune responses and inflammation. Recently, NF-KB has generated considerable interest as it implicated in human cancer initiation, progression and resistance of treatment. The NF-KB can be activated by various intra- and extra-cellular stimuli, such as cytokines, oxidant-free radicals, ultraviolet irradiation, bacterial and viral products. Activated NF-KB translocates into the nucleus and stimulates gene expression involved in a wide variety of biological functions. Inappropriate activation of NF-KB has been associated with various inflammatory diseases, while persistent inhibition of NF-KB leads to inappropriate immune cell development or delayed cell growth. Nevertheless, NF-KB is a critical regulator of the immediate-early response to viral infection.

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More information About NF-KB

NF-KB Channel Characteristics

Irregular activation of the Nuclear Factor Kappa-B (NF-KB) transcription system contributes to cancer progression and threatens bone health. Several major components of the NF-KB pathway, such as NF-KB1 and NF-KB2 subunits, can stimulate the transcription of proliferation regulating genes (e.g., cyclin D1 and c-myc) involved in metastasis, VEGF-dependent angiogenesis and cell immortality. Furthermore, NF-KB activation can also induce the expression of cytidine deaminase (AID) and APOBEC proteins, creating a mechanistic link between the NF-KB pathway and mutagenic characteristics of cervical cancer. Inhibition of NF-KB can potentially be used to reverse resistance to radiotherapy and systemic anti-cancer medication, but no clinically proven NF-KB targeting strategy is available currently.

NF-KB Channel Inhibitor

The Nuclear Factor Kappa-B (NF-KB) is essential for coordinating inflammatory responses, including innate immunity, adaptive immunity, cellular differentiation, proliferation, and survival in almost all multicellular organisms. Therefore, the NF-KB system is tightly regulated, and irregulation of NF-KB has been implicated in a wide range of diseases ranging from inflammatory and immune disorders to cancers. As a result, the NF-KB regulatory network and its dynamics offer a multitude of promising therapeutic targets that remain to be fully explored and translated into clinical use. However, to untapped the potential for finer-grained therapeutic targeting of the NF-KB signaling system requires a quantitative understanding of dynamical control and integration of various physiological and pathological signals and stimuli. Aeruginosin-865 (Aer-865), isolated from the terrestrial cyanobacterium Nostoc sp, is the first aeruginosin-type peptide containing both fatty acid and a carbohydrate moiety. Confocal laser scanning microscopy revealed that the anti-inflammatory effect of Aer-865 was directly associated with inhibition of NF-KB translocation to the nucleus.

References:

  1. Hoffmann, A.; et al.Signaling via the NF-KB system. WIREs Syst Biol Med, 2016, 8:227-241.
  2. Hrouzek, P.; et al. Novel Aeruginosin-865 from Nostoc sp. as a Potent Anti-inflammatory Agent. Chem. Bio. Chem., 2013, 14: 2329-2337.
* Only for research. Not suitable for any diagnostic or therapeutic use.

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