PACSIN1

Official Full Name

protein kinase C and casein kinase substrate in neurons 1

Organism

Homo sapiens

GeneID

29993

Background

Enables phospholipid binding activity. Involved in plasma membrane tubulation. Located in cytoplasm. [provided by Alliance of Genome Resources, Feb 2025]

Synonyms

SDPI;

Cat.No.	Product Name	Price

Cat.No.	Product Name	Price

Cat.No.	Product Name	Price

Cat.No.	Product Name	Price

Detailed Information

Pacsin1 works as a AMPA receptor trafficking dynamics regulator

In the mammalian central nervous system, AMPA receptors (AMPARs) role as the main ionotropic glutamate receptors for the fast excitatory neurotransmission. Synaptic plasticity, a cellular correlate of learning and memory, can be regulated by them due to its mobility and transportation into and out of synapses. Multiple forms of synaptic plasticity can regulate AMPARs traffic between intracellular compartments and plasma membrane via receptor endocytosis, endosomal trafficking, recycling and exocytosis. A net AMPAR increase may forward trafficking toward the plasma membrane and synaptic to form a long-term potentiation, and AMPARs removal from cell surface can induce synaptic strength weakness and long-term depression (LTD).

F-BAR (elongated BAR) and SH3 (src homology-3) domain-containing protein, the Sindarin, also known as protein kinase C and casein kinase II substrate in neurons (PACSIN), is capable of plasma membrane remodeling and protein-protein interactions mediation. In activity-dependent endocytosis regulation and presynaptic vesicles recycle, PACSIN also contributed a lot, as well as postsynaptic AMPA, NMDA and glycine receptors. In its interactions with PICK1, PACSIN can regulate the activity-dependent removal of AMPRs from the plasma membrane. And cerebellar LTD impairment can be led by the PACSIN function loss or PACSIN-PICK1 interaction inhibition. A pH-sensitive green fluorescent protein, phogrin, which can be tagged to the extracellular domain of the GluA2 subunit of AMPARs, was used to reveal the molecular mechanism by which PACSIN regulates the dynamics of AMPAR trafficking. It was demonstrated that PACSIN1 works as a versatile membrane deformation protein that has linkage with endocytic and recycling machineries essential for dynamic AMPAR trafficking in neurons.

Pacsin1 works as a regulator of TLR7/9-mediated type I interferon response in plasmacytoid dendritic cells

As the professional interferon (IFN)-producing cells of the immune system, with specifically expression of Toll-like receptor (TLR)7 and TLR9 molecules, Plasmacytoid dendritic cells (pDCs) can produce massive amounts of type I IFN by sensing microbial nucleic acids via TLR7 and TLR9. The knockdown of protein kinase C and casein kinase substrate in neurons, which is also known as Pacsin1 specifically expressed in plasmacytoid dendritic cells, can significantly inhibit the type I IFN response of the pDCs to TLR9 ligand.

PACSIN1 Figure 1. Dynamics of AMPA receptor trafficking regulated by PACSIN1. (Jocelyn Widagdo, et al. 2016)

References:

Widagdo J, Fang H, Jang S E, et al. PACSIN1 regulates the dynamics of AMPA receptor trafficking. Scientific reports, 2016, 6(1): 1-9.
Esashi E, Bao M, Wang Y H, et al. PACSIN1 regulates the TLR7/9‐mediated type I interferon response in plasmacytoid dendritic cells. European journal of immunology, 2012, 42(3): 573-579.

Quick Inquiry

Interested in learning more?

Contact us today for a free consultation with the scientific team and discover how Creative Biogene can be a valuable resource and partner for your organization.

Request a quote today!

Inquiry