The Role of LNK (SH2B3) in the Regulation of JAK-STAT Signalling in Haematopoiesis

被引：21

作者：

Morris, Rhiannon ^{[1
,2
]}

Butler, Liesl ^{[3
,4
]}

Perkins, Andrew ^{[3
,4
]}

Kershaw, Nadia J. ^{[1
,2
]}

Babon, Jeffrey J. ^{[1
,2
]}

机构：

[1] Walter & Eliza Hall Inst Med Res, Parkville, Vic 3052, Australia

[2] Univ Melbourne, Dept Med Biol, Parkville, Vic 3052, Australia

[3] Monash Univ, Australian Ctr Blood Dis, Melbourne, Vic 3001, Australia

[4] Alfred Hlth, Melbourne, Vic 3001, Australia

来源：

PHARMACEUTICALS | 2022年 / 15卷 / 01期

基金：

澳大利亚国家健康与医学研究理事会; 英国医学研究理事会;

关键词：

JAK-STAT; myeloproliferative neoplasms; ADAPTER PROTEIN; MYELOPROLIFERATIVE NEOPLASMS; PLECKSTRIN HOMOLOGY; GENETIC ALTERATIONS; STRUCTURAL BASIS; SELF-RENEWAL; STEM-CELLS; MUTATIONS; MPL; ACTIVATION;

D O I：

10.3390/ph15010024

中图分类号：

R914 [药物化学];

学科分类号：

100701 ;

摘要：

LNK is a member of the SH2B family of adaptor proteins and is a non-redundant regulator of cytokine signalling. Cytokines are secreted intercellular messengers that bind to specific receptors on the surface of target cells to activate the Janus Kinase-Signal Transducer and Activator of Transcription (JAK-STAT) signalling pathway. Activation of the JAK-STAT pathway leads to proliferative and often inflammatory effects, and so the amplitude and duration of signalling are tightly controlled. LNK binds phosphotyrosine residues to signalling proteins downstream of cytokines and constrains JAK-STAT signalling. Mutations in LNK have been identified in a range of haematological and inflammatory diseases due to increased signalling following the loss of LNK function. Here, we review the regulation of JAK-STAT signalling via the adaptor protein LNK and discuss the role of LNK in haematological diseases.

引用

页数：10

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