Anti-STEP / PTPN5 antibody

Supplementary info

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

Activity summary

STEP also known as PTPN5 is a protein tyrosine phosphatase with a molecular mass approximately 69-80 kDa. It regulates the activity of key signaling proteins by dephosphorylation. Expression of STEP occurs mainly in the central nervous system particularly in the striatum hippocampus and cortex regions of the brain. These areas of expression suggest its significant role in neuronal signaling and function. STEP exists in multiple isoforms which allow it to participate in various signaling pathways by altering substrate specificity.

Biological function summary

STEP plays a significant role in modulating synaptic strength and plasticity acting as a negative regulator of synaptic signaling. Its main function involves dephosphorylating several kinase substrates like ERK1/2 and Fyn kinase thereby reducing their activity. This action controls synaptic sensitivity to neurotransmitters and impacts long-term potentiation a process essential for learning and memory. STEP does not form part of a large complex but interacts with other proteins through transient associations based on cellular needs.

Pathways

STEP contributes significantly to the glutamatergic and dopaminergic signaling pathways. Within these pathways STEP dephosphorylates and inactivates specific receptors and kinases to maintain homeostasis in neuronal signaling. For example in the glutamatergic pathway STEP deactivates NMDA receptors affecting calcium influx and signaling cascades that rely on it. Its interactions with other proteins like ERK which is part of the MAPK pathway illustrate its integrated role in signal transduction cascades that influence cellular responses to neurotransmitters.

Associated diseases and disorders

STEP has a relationship with neurodegenerative diseases such as Alzheimer's disease and schizophrenia. Increased activity of STEP leads to excessive dephosphorylation of proteins necessary for synaptic function contributing to the cognitive deficits observed in these disorders. In Alzheimer's disease for instance hyperactive STEP decreases the phosphorylation of the NMDA receptor and disrupts synaptic transmission. Additionally STEP's influence extends to dynamin-related protein 1 (Drp1) in neurodegenerative pathways indicating how altered STEP activity can escalate mitochondrial dysfunction commonly seen in Alzheimer's pathology.