The SHP2-ERK2 signaling pathway regulates branched I antigen formation by controlling the binding of CCAAT/enhancer binding protein α to the IGnTC promoter region during erythroid differentiation

Yi Jen Liao, Yen Hua Lee, Fu Ling Chang, Hsun Ho, Chin Han Huang, Yuh Ching Twu

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

BACKGROUND: Phosphorylation status of the transcription factor CCAAT/enhancer binding protein α (C/EBPα) has been demonstrated in a human hematopoietic cell model to regulate the formation of branched I antigen by affecting its binding affinity to the promoter region of the IGnTC gene during erythroid and granulocytic differentiation. STUDY DESIGN AND METHODS: The K-562 cell line was induced to differentiate into red blood cells (RBCs) or granulocytes by sodium butyrate or retinoic acid, respectively, to study the involvement of three MAP kinase pathways in I antigen synthesis. The regulatory effects of the extracellular signal-regulated kinase (ERK)2-Src homology region 2 domain-containing phosphatase 2 (SHP2) pathway on phosphorylation status and binding affinities of C/EBPα as well as the subsequent activation of IGnTC and synthesis of surface I formation were studied in wild-type K-562 cells and in mutant cells that overexpress ERK2 and SHP2. RESULTS: We found that SHP2-ERK2 signaling regulates the phosphorylation status of C/EBPα to alter its binding affinity onto the IGnTC promoter region, thereby activating the synthesis of cell surface I antigen formation during erythropoiesis. CONCLUSION: SHP2-ERK2 signaling acts upstream of C/EBPα as a regulator of cell surface I antigen synthesis. Such regulation is specific for RBC but not for granulocyte differentiation.

Original languageEnglish
Pages (from-to)2691-2702
Number of pages12
JournalTransfusion
Volume56
Issue number11
DOIs
Publication statusPublished - Nov 1 2016

Fingerprint

CCAAT-Enhancer-Binding Proteins
Genetic Promoter Regions
Phosphorylation
Surface Antigens
Granulocytes
SH2 Domain-Containing Protein Tyrosine Phosphatases
Erythrocytes
Butyric Acid
src Homology Domains
Erythropoiesis
Mitogen-Activated Protein Kinase 1
Tretinoin
Transcription Factors
Phosphotransferases
Cell Line
I-antigen
Genes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Hematology

Cite this

The SHP2-ERK2 signaling pathway regulates branched I antigen formation by controlling the binding of CCAAT/enhancer binding protein α to the IGnTC promoter region during erythroid differentiation. / Liao, Yi Jen; Lee, Yen Hua; Chang, Fu Ling; Ho, Hsun; Huang, Chin Han; Twu, Yuh Ching.

In: Transfusion, Vol. 56, No. 11, 01.11.2016, p. 2691-2702.

Research output: Contribution to journalArticle

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abstract = "BACKGROUND: Phosphorylation status of the transcription factor CCAAT/enhancer binding protein α (C/EBPα) has been demonstrated in a human hematopoietic cell model to regulate the formation of branched I antigen by affecting its binding affinity to the promoter region of the IGnTC gene during erythroid and granulocytic differentiation. STUDY DESIGN AND METHODS: The K-562 cell line was induced to differentiate into red blood cells (RBCs) or granulocytes by sodium butyrate or retinoic acid, respectively, to study the involvement of three MAP kinase pathways in I antigen synthesis. The regulatory effects of the extracellular signal-regulated kinase (ERK)2-Src homology region 2 domain-containing phosphatase 2 (SHP2) pathway on phosphorylation status and binding affinities of C/EBPα as well as the subsequent activation of IGnTC and synthesis of surface I formation were studied in wild-type K-562 cells and in mutant cells that overexpress ERK2 and SHP2. RESULTS: We found that SHP2-ERK2 signaling regulates the phosphorylation status of C/EBPα to alter its binding affinity onto the IGnTC promoter region, thereby activating the synthesis of cell surface I antigen formation during erythropoiesis. CONCLUSION: SHP2-ERK2 signaling acts upstream of C/EBPα as a regulator of cell surface I antigen synthesis. Such regulation is specific for RBC but not for granulocyte differentiation.",
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AU - Ho, Hsun

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