MW 271.78 Da, Purity >99%. Potent non-selective β adrenoceptor antagonist (Ki values are 5.2, 50 and 170 nM at β2, β1 and β3, respectively). Similar potency to propranolol (ab120757).
AP-1, Activator protein 1, Enhancer Binding Protein AP1, JUN protein, JUNC, JUN_HUMAN, Jun Activation Domain Binding Protein, Jun oncogene, Jun proto oncogene, Oncogene JUN, Proto-oncogene c-jun, Transcription factor AP-1, V jun sarcoma virus 17 oncogene homolog, V jun sarcoma virus 17 oncogene homolog (avian), V-jun avian sarcoma virus 17 oncogene homolog, cJun, p39
MW 271.78 Da, Purity >99%. Potent non-selective β adrenoceptor antagonist (Ki values are 5.2, 50 and 170 nM at β2, β1 and β3, respectively). Similar potency to propranolol (ab120757).
Soluble in DMSO to 100 mM.
Soluble in ethanol to 100 mM.
Potent non-selective β adrenoceptor antagonist (Ki values are 5.2, 50 and 170 nM at β2, β1 and β3, respectively). Similar potency to propranolol (ab120757).
The protein c-Jun is an important component of the AP-1 transcription factor complex and is often referred to by alternative names such as c-jun. It has a molecular weight of about 39 kDa. Scientists have found c-jun expressed in a wide range of tissues indicating its diverse roles in cellular functions. This protein plays a critical mechanical role by binding specific DNA sequences to regulate the transcription of various genes involved in cell proliferation and apoptosis.
C-Jun impacts cellular activities by being a significant part of the AP-1 transcription factor complex interacting with other proteins such as Fos. This interaction allows c-Jun to modulate gene expression in response to cellular stimuli. In particular c-Jun influences cell cycle progression and differentiation. Therefore its activity is necessary for physiological and pathological processes. As c-jun's function remains tightly regulated any changes can have wide-ranging effects.
C-Jun significantly influences the MAPK/ERK and JNK pathways. These pathways play important roles in cellular responses to stress growth factors and cytokines. Within these pathways c-Jun interacts with proteins such as JNK which phosphorylates c-Jun and enhances its activity. These interactions allow c-Jun to regulate target genes involved in important cellular processes without much delay. Understanding c-Jun's function in these pathways helps elucidate how cells control division survival and apoptosis.
C-Jun's dysregulation connects to various conditions including cancer and neurodegenerative diseases. Abnormal c-Jun activity can lead to oncogenesis by promoting unrestrained cellular proliferation. Additionally c-Jun involvement in disorders like Alzheimer's disease stems from its role in apoptotic pathways which may cause neuronal death. Accompanying proteins like JNK are also implicated in these conditions making the regulation and expression of c-Jun a focus for therapeutic research.
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2D chemical structure image of ab141132, Bupranolol, beta adrenoceptor antagonist
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