{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chowdhury S"],"funding":["DST | Science and Engineering Research Board","DST | Science and Engineering Research Board (SERB)","DBT/Wellcome Trust India Alliance","Wellcome Trust"],"pagination":["2181-2195"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12380609"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["39(9)"],"pubmed_abstract":["The maintenance of the haematopoietic stem cells and the production of platelets thereof is acutely dependent upon the thrombopoietin receptor (TpoR). TpoR dimerizes in the presence of its ligand thrombopoietin leading to the activation of downstream JAK2-STAT signalling. Alternatively, the receptor dimerizes in the presence of activating mutations of JAK2 (JAK2 V617F), calreticulin or TpoR leading to myeloproliferation. These effects are dependent upon the surface expression of the receptor. TpoR is secreted through the Golgi-dependent pathway. Although, an unconventional autophagosome-lysosome mediated traffic has been postulated; questions remained whether the observed lysosomal localization was indicative of degradation or secretion. We fused the pH-sensitive FRET pair of TOLLES-YPet w"],"journal":["Leukemia"],"pubmed_title":["Autophagosome-lysosome mediated secretion of the thrombopoietin receptor is modulated by distinct driver mutations of myeloproliferative neoplasm."],"pmcid":["PMC12380609"],"funding_grant_id":["CRG/2023/003853","IA/I/19/1/504285"],"pubmed_authors":["Naseer S","Shrivastva S","Chowdhury S","Singh A","Roy A","Ansari F"],"additional_accession":[]},"is_claimable":false,"name":"Autophagosome-lysosome mediated secretion of the thrombopoietin receptor is modulated by distinct driver mutations of myeloproliferative neoplasm.","description":"The maintenance of the haematopoietic stem cells and the production of platelets thereof is acutely dependent upon the thrombopoietin receptor (TpoR). TpoR dimerizes in the presence of its ligand thrombopoietin leading to the activation of downstream JAK2-STAT signalling. Alternatively, the receptor dimerizes in the presence of activating mutations of JAK2 (JAK2 V617F), calreticulin or TpoR leading to myeloproliferation. These effects are dependent upon the surface expression of the receptor. TpoR is secreted through the Golgi-dependent pathway. Although, an unconventional autophagosome-lysosome mediated traffic has been postulated; questions remained whether the observed lysosomal localization was indicative of degradation or secretion. We fused the pH-sensitive FRET pair of TOLLES-YPet w","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-05-10T04:39:40.29Z","creation":"2026-04-08T01:30:55.783Z"},"accession":"S-EPMC12380609","cross_references":{"pubmed":["40610764"],"doi":["10.1038/s41375-025-02676-6"]}}