POSH undergoes phase separation and co-condensation with SHANK2/3 to regulate spine development

Minghui Yao , Ling Yuan , Yu Zheng , Zhiheng Xu

Protein Cell ›› 2026, Vol. 17 ›› Issue (1) : 77 -82.

PDF (1225KB)
Protein Cell ›› 2026, Vol. 17 ›› Issue (1) :77 -82. DOI: 10.1093/procel/pwaf066
Letter
POSH undergoes phase separation and co-condensation with SHANK2/3 to regulate spine development
Author information +
History +
PDF (1225KB)

Graphical abstract

Cite this article

Download citation ▾
Minghui Yao, Ling Yuan, Yu Zheng, Zhiheng Xu. POSH undergoes phase separation and co-condensation with SHANK2/3 to regulate spine development. Protein Cell, 2026, 17(1): 77-82 DOI:10.1093/procel/pwaf066

登录浏览全文

4963

注册一个新账户 忘记密码

References

[1]

Baron MK , Boeckers TM , Vaida B et al. An architectural framework that may lie at the core of the postsynaptic density. Science 2006; 311: 531– 535.

[2]

Boeckers TM , Liedtke T , Spilker C et al. C‐terminal synaptic targeting elements for postsynaptic density proteins ProSAP1/Shank2 and ProSAP2/Shank3. J Neurochem 2005; 92: 519– 524.

[3]

Durand CM , Betancur C , Boeckers TM et al. Mutations in the gene encoding the synaptic scaffolding protein SHANK3 are associated with autism spectrum disorders. Nat Genet 2007; 39: 25– 27.

[4]

Fourie C , Vyas Y , Lee K et al. Dietary zinc supplementation prevents autism related behaviors and striatal synaptic dysfunction in Shank3 Exon 13–16 mutant mice. Front Cell Neurosci 2018; 12: 374.

[5]

Grabrucker S , Jannetti L , Eckert M et al. Zinc deficiency dysregulates the synaptic ProSAP/Shank scaffold and might contribute to autism spectrum disorders. Brain 2014; 137: 137– 152.

[6]

Guo B , Chen J , Chen Q et al. Anterior cingulate cortex dysfunction underlies social deficits in Shank3 mutant mice. Nat Neurosci 2019; 22: 1223– 1234.

[7]

Leblond CS , Nava C , Polge A et al. Meta-analysis of SHANK Mutations in Autism Spectrum Disorders: a gradient of severity in cognitive impairments. PLoS Genet 2014; 10: e1004580.

[8]

Lee E-J , Lee H , Huang T-N et al. Trans-synaptic zinc mobilization improves social interaction in two mouse models of autism through NMDAR activation. Nat Commun 2015; 6: 7168.

[9]

Mei Y , Monteiro P , Zhou Y et al. Adult restoration of Shank3 expression rescues selective autistic-like phenotypes. Nature 2016; 530: 481– 484.

[10]

Moessner R , Marshall CR , Sutcliffe JS et al. Contribution of SHANK3 mutations to autism spectrum disorder. Am J Hum Genet 2007; 81: 1289– 1297.

[11]

Monteiro P , Feng G SHANK proteins: roles at the synapse and in autism spectrum disorder. Nat Rev Neurosci 2017; 18: 147– 157.

[12]

Satterstrom FK , Kosmicki JA , Wang J et al. Large-scale exome sequencing study implicates both developmental and functional changes in the neurobiology of autism. Cell 2020; 180: 568– 584.e23.

[13]

Sieme D , Engelke M , Rezaei-Ghaleh N et al. Autoinhibition in the signal transducer CIN85 modulates B cell activation. J Am Chem Soc 2024; 146: 399– 409.

[14]

Yao M , Meng M , Yang X et al. POSH regulates assembly of the NMDAR/PSD-95/Shank complex and synaptic function. Cell Rep 2022; 39: 110642.

[15]

Zeng M , Chen X , Guan D et al. Reconstituted postsynaptic density as a molecular platform for understanding synapse formation and plasticity. Cell 2018; 174: 1172– 1187.e16.

RIGHTS & PERMISSIONS

© The Author(s) 2025. Published by Oxford University Press on behalf of Higher Education Press.

PDF (1225KB)

Supplementary files

Supplementary_Figures_S1-S4

Supplementary_Movies_S1

28

Accesses

0

Citation

Detail

Sections
Recommended

/