Publication for Cct5 and Tcp1

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	Cct5	chaperonin containing Tcp1, subunit 5 (epsilon)	12465			[link]
mmu	Tcp1	t-complex protein 1	21454

Pubmed ID	Priority	Text
30632495	0.98	CCT subunit (CCT5) significantly promoted retrograde axonal transport of brain-derived neurotrophic factor in primary cortical neurons.
	0.98	CCT5 on retrograde axonal transport, which highlights the differential regulation of tauWT and tauP301L by CCT subunit (Chen et al., 2018b).
	0.98	CCT5 overexpression significantly increased the level of CDK5/p35/p25, contributing towards CCT-induced tau phosphorylation.
	0.98	CCT complex modulates ~10% of the eukaryotic proteins, raising the possibility that other glycogen synthase kinase 3beta effectors might be potentially affected and interact with the CDK5 pathway to enhance the CCT5-mediated beneficial effect on axonal transport.
	0.97	CCT5 on tau phosphorylation requires an oligomeric complex that is either self-assembled by transfected CCT5 or assembled by CCT5 with other endogenous CCT subunits.
	0.97	CCT-promoted axonal transport in neurodegenerative diseases: In our previous study, both CCT3 and CCT5 rescued the axonal transport deficit in mutant Huntingtin-expressing neurons from an Huntington's disease mouse model.
	0.96	CCT-induced increase of CDK5/p35 required tau expression (Chen et al., 2018b), the effect of CCT5 on the retrograde axonal transport of brain-derived neurotrophic factor may arise from either tau-dependent mechanism(s) or indirect mechanism(s) including CDK5-mediated Ndel1 phosphorylation or both.
	0.95	CCT subunit modulates retrograde axonal transport in a tau-dependent manner: Lentivirus-mediated upregulation of CCT5 in primary cortical neurons resulted in an increase in instantaneous velocity (the absolute velocity calculated from moving time without pause time included) and a decrease in both the percentage of pause events and average pause duration of retrograde brain-derived neurotrophic factor axonal transport in microfluidic chamber.
	0.77	CCT5 did not affect the level of other CCT subunits (Chen et al., 2018b).
28553203	0.98	CCT integrity by knock-down or by mutations in CCT5 disrupts autolysosome formation and cargo degradation.
	0.90	TCP1 subunit 5 (CCT5) on the other hand inhibits the degradation step.
29312475	0.98	TCP1 complex (Cct1-3 and Cct5) (Table 1).
29531365	0.97	CCT1, CCT2, CCT3, CCT4, CCT5, and CCT8) displayed median robust Z-scores less than -2.5, implicating this host chaperonin in viral replication (Fig. 1e).
30543055	0.97	CCT5, GRP78, PDIA6, PRDX4 and TCP1 (Table 2; Fig. 4c; full MS analysis in Online Resource 3).
23637185	0.95	CCTepsilon and the CCT substrate beta-actin was unchanged in the PhLP1 knockout rods, again indicating that the effects of PhLP1 deletion were specific to G proteins.
	0.94	CCTepsilon subunit in the retina was unchanged with loss of PhLP1 as was expression of two important CCT substrates, beta-actin and beta-tubulin.