PACSIN2

Official Full Name

protein kinase C and casein kinase substrate in neurons 2

Organism

Homo sapiens

GeneID

11252

Background

This gene is a member of the protein kinase C and casein kinase substrate in neurons family. The encoded protein is involved in linking the actin cytoskeleton with vesicle formation by regulating tubulin polymerization. Alternative splicing results in multiple transcript variants. [provided by RefSeq, May 2010]

Synonyms

SDPII;

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Detailed Information

Pacsin2 works as a HIV-1 carrier for cell-to-cell spread

Popov published a paper in PANS has shown that recruitment of cellular protein Pacsin2 into the sites of assembly for virus spread promotion at points of cell-to-cell contact can be done by the HIV-1 Gag ubiquitin modification. Several respects outstand the significance of this finding. First, Pacsin2 was identified as a host factor and vital mediator for HIV-1 cell-to-cell transfer. The new date of Popov suggested that bridge between Gag and actin can facilitate the process of actin reorganization at the VS. Second, Gag-ubiquitin conjugates were a heretofore unappreciated function for cellular machinery that can enhance HIV-1 replication. Third, this study underscores the importance of cell-to-cell transfer in HIV-1 spread by the in vitro experiment. Besides the in-measurable effect of Pacsin2 depletion on virus particle assembly and release or virion infectivity, spreading infection establishment can be effectively shut down by it.

Pacsin2-depenent and clathrin-indepenent endocytosis was undergone by clostridium difficile Toxin A

Clostridium difficile infection has a high rate in the United States hospitalized patients, and the two homologous exotoxins, TcdA and TcdB, role as the major virulence factors in C. difficile pathogenesis. Host cellular function disruption, induction of fluid secretion, inflammation, and cell death can be induced by the toxins mediated Rho family GTPases inactivation. A combination of RNAi-based knockdown, pharmacological inhibition, and cell imaging approaches were utilized to investigate the mechanism of TcdA uptake and subsequent cytopathic and cytotoxic effects. More than this, fluorescently labeled TcdA in confocal microscopy, a colocalization of the toxin with Pacsin2-positive structures in cells during entry can be seen. RNAi-based knockdown approaches inhibited TcdA uptake and toxin-induced downstream effects in cells gave an indication that TcdA entry is Pacsin2-dependent. So, it can be easily concluded that TcdA and TcdB can utilize distinct endocytic mechanisms to intoxicate host cells.

PACSIN2 Figure 1. PACSIN2 work as a package for HIV-1 spreading from cell-to-cell. (Rachel Van Duyne, et al. 2018)

References:

Van Duyne R, Freed E O. HIV-1 packs in PACSIN2 for cell-to-cell spread. Proceedings of the National Academy of Sciences, 2018, 115(27): 6885-6887.
Chandrasekaran R, Kenworthy A K, Lacy D B. Clostridium difficile toxin A undergoes clathrin-independent, PACSIN2-dependent endocytosis. PLoS pathogens, 2016, 12(12): e1006070.

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