APC Anti-CREB (phospho S133) antibody [CREBS133-4D11]

Supplementary info

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

Activity summary

CAMP response element-binding protein better known as CREB functions as a transcription factor that regulates gene expression. CREB protein operates by binding to specific DNA sequences called cAMP response elements in the promoters of target genes leading to increased or altered transcription. The protein has a molecular weight around 43 kDa. Expressed broadly in many tissues CREB's activity is particularly high in the brain where it plays key roles in neuronal functions. Researchers also refer to phospho-CREB when discussing the activated form of this protein often analyzed through methods like CREB Western blot.

Biological function summary

CREB contributes significantly to cellular processes such as proliferation differentiation and survival through transcriptional regulation. CREB does not function alone; it frequently associates with other proteins forming complexes to exert its regulatory roles. Additionally CREB influences the development of memory and learning in neurons highlighting its extensive involvement in neurophysiological processes.

Pathways

CREB plays a substantial role in the cAMP signaling pathway as well as the mitogen-activated protein kinase (MAPK) pathway. Through its interaction with kinases and other signaling proteins CREB influences numerous downstream targets affecting cellular responses to external stimuli. Notably protein kinase A (PKA) activates CREB by phosphorylation facilitating its role in various signal transduction pathways and linking it to downstream transcriptional events.

Associated diseases and disorders

Research links CREB to neurological disorders and some forms of cancer. Aberrant CREB activity associates with neurodegenerative diseases like Alzheimer’s where dysregulated gene expression impacts neuronal viability and function. Furthermore in cancer CREB's role in cell proliferation and survival ties it to oncogenes such as BCL2 where abnormal CREB function can promote tumorigenesis. Understanding these connections provides valuable insights for therapeutic strategies against such diseases.