ELM - instance LIG_EABR_CEP55_1 in sequence Q7M6U3 at position 788

Instance

Accession	Acc. Gene-, Name	Start	End	Subsequence	Logic	PDB	Organism	Length
ELMI002464	Q7M6U3 Tex14 TEX14_MOUSE	788	798	AKFQPAVGPPSLAYLPPVMQ	TP	---	Mus musculus (House mouse)	1450

Instance evidence

Evidence class	PSI-MI	Method	BioSource	PubMed	Logic	Reliability	Notes
experimental	MI:0728	gal4 vp16 complementation	in vitro	Iwamori,2010	support	certain	InteractionDetection
experimental	MI:0007	anti tag coimmunoprecipitation	in vivo	Iwamori,2010	support	certain	InteractionDetection
experimental	MI:0018	two hybrid	in vivo	Iwamori,2010	support	certain	InteractionDetection
experimental	MI:0405	competition binding	in vitro	Iwamori,2010	support	certain	InteractionDetection
experimental	MI:0074	mutation analysis	in vivo/in vitro	Iwamori,2010	support	certain	FeatureDetection

Interactions

Uniprot Id	Domain family	Domain Start	Domain End	Affinity Min/Max (µMol)	Notes
(Q8BT07) CEP55_MOUSE	PF12180 (EABR) TSG101 and ALIX binding domain of CEP55	171	205		[mitab][xml]

Switches

This ELM instance is part of the following 2 switching mechanisms annotated at the switches.ELM resource:

SWTI000331:

The switch from cytokinesis to intracellular bridge formation in differentiating male germ cells is mediated by Testis-expressed protein 14 (Tex14). Binding of Tex14 to Centrosomal protein of 55 kDa (Cep55) prevents binding of ALIX (Programmed cell death 6-interacting protein (Pdcd6ip)) and Tumor susceptibility gene 101 protein (Tsg101) to Cep55, which is required for abscission at the end of cytokinesis. Tex14 uses the same site on Cep55 as ALIX (Pdcd6ip) and Tsg101. The strong interaction between Tex14 and Cep55 together with the avidity effect that results from interaction of MKLP1 with both Tex14 and Cep55 prevent recruitment of ALIX (Pdcd6ip) and Tsg101 for abscission.
SWTI000332:

The switch from cytokinesis to intracellular bridge formation in differentiating male germ cells is mediated by Testis-expressed protein 14 (Tex14). Binding of Tex14 to Centrosomal protein of 55 kDa (Cep55) prevents binding of ALIX (Programmed cell death 6-interacting protein (Pdcd6ip)) and Tumor susceptibility gene 101 protein (Tsg101) to Cep55, which is required for abscission at the end of cytokinesis. Tex14 uses the same site on Cep55 as ALIX (Pdcd6ip) and Tsg101. The strong interaction between Tex14 and Cep55 together with the avidity effect that results from interaction of MKLP1 with both Tex14 and Cep55 prevent recruitment of ALIX (Pdcd6ip) and Tsg101 for abscission.

Please cite: ELM-the Eukaryotic Linear Motif resource-2024 update. (PMID:37962385)

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