ELM - instance LIG_SH2_STAT5 in sequence P16471 at position 342

Instance

Accession	Acc. Gene-, Name	Start	End	Subsequence	Logic	PDB	Organism	Length
ELMI000426	P16471 PRLR PRLR_HUMAN	342	345	PSQGMKPTYLDPDTDSGRGS	U	---	Homo sapiens (Human)	622

Instance evidence

Evidence class	PSI-MI	Method	BioSource	PubMed	Logic	Reliability	Notes
experimental	MI:0074	mutation analysis	in vivo/in vitro	Lebrun,1995	support	certain	FeatureDetection

Switches

This ELM instance is part of the following 1 switching mechanism annotated at the switches.ELM resource:

SWTI000626:

Alternative Splicing removes the degron motif of Prolactin receptor (PRLR), abrogating binding to Signal transducer and activator of transcription 5A (STAT5A). The PRLR S1a (Isoform Short form 1a) and S1b and (Isoform Short form 1b) isoforms were unable to mediate the transcriptional activation of the beta-casein promoter via the JAK-STAT5 pathway. Therefore these two splice variants act as dominant negatives on the full-length version LF (Isoform 1). Another study showed that different splice variants of heterodimers (e.g. LF/S1a, LF/S1b) that were able to induce JAK2 phosphorylation but not further signalling events due to lack of STAT recruitment (Qazi et al. (2006) (here)).

Pathways

KEGG: The sequence P16471 is implicated in the following 5 Pathways: (color codes: This sequence=red, interacting sequence=orange)

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

ELM data can be downloaded & distributed for non-commercial use according to the ELM Software License Agreement