Anti-c-Jun (phospho T91) antibody [EPR2236] - BSA and Azide free

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

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.

Biological function summary

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.

Pathways

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.

Associated diseases and disorders

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.