THE SHP-2/ERK2-MEDIATED SIGNALING REGULATES BRANCHED I FORMATION BY CONTROLLING THE C/EBPΑ BINDING TO IGNTC PROMOTER REGION IN THE ERYTHROID-DIFFERENTIATION
(Abstract release date: 05/19/16)
EHA Library. Twu Y. 06/09/16; 133118; E1569
Dr. Yuh-Ching Twu
Contributions
Contributions
Abstract
Abstract: E1569
Type: Eposter Presentation
Background
The straight and branched repeats of poly-LacNAc chains characterize the histo-blood group i and I antigens, respectively. In the human hematopoietic cell model, the transcription factor CCAAT/enhancer binding protein a (C/EBPa) regulates branched I antigen formation through IGnTC expression in both erythroid- and granulocytic-differentiation. However, the detail mechanisms for the regulation on the I synthesis along these different lineages remain unclear.
Aims
To investigate the regulatory mechanisms for branched I antigen formation during the erythroid- and granulocytic-differentiation.
Methods
The sodium butyrate (SB)- and retinoic acid (RA)-induced differentiated K-562 cells were served as the erythroid- and granulocytic-differentiation model, respectively. The wild type and mutant form of ERK2 and SHP-2-overexpressing K-562 cells were used to study the involvement of MAP kinase-mediated pathways and upstream signaling molecule in the I antigen formation. CHIP analysis was used to compare the binding affinity of C/EBPa to IGnTC promoter.
Results
The ERK2-mediated signaling specifically regulated the synthesis of I antigens during the erythroid-differentiation, but not for granulocytic-differentiation. SHP-2 acted as upstream regulator of ERK2 to control the phosphorylation status of Ser21 on C/EBPa, which affect the binding affinity to IGnTC regulatory region, and to govern the I antigen formation.
Conclusion
In this K-562 cell model when induced by SB, the SHP-2-ERK2 signaling is specific for the branched poly-LacNAc formation during erythroid-differentiation.
Session topic: E-poster
Keyword(s): C/EBP, ERK, Erythroid differentiation, SHP-2
Type: Eposter Presentation
Background
The straight and branched repeats of poly-LacNAc chains characterize the histo-blood group i and I antigens, respectively. In the human hematopoietic cell model, the transcription factor CCAAT/enhancer binding protein a (C/EBPa) regulates branched I antigen formation through IGnTC expression in both erythroid- and granulocytic-differentiation. However, the detail mechanisms for the regulation on the I synthesis along these different lineages remain unclear.
Aims
To investigate the regulatory mechanisms for branched I antigen formation during the erythroid- and granulocytic-differentiation.
Methods
The sodium butyrate (SB)- and retinoic acid (RA)-induced differentiated K-562 cells were served as the erythroid- and granulocytic-differentiation model, respectively. The wild type and mutant form of ERK2 and SHP-2-overexpressing K-562 cells were used to study the involvement of MAP kinase-mediated pathways and upstream signaling molecule in the I antigen formation. CHIP analysis was used to compare the binding affinity of C/EBPa to IGnTC promoter.
Results
The ERK2-mediated signaling specifically regulated the synthesis of I antigens during the erythroid-differentiation, but not for granulocytic-differentiation. SHP-2 acted as upstream regulator of ERK2 to control the phosphorylation status of Ser21 on C/EBPa, which affect the binding affinity to IGnTC regulatory region, and to govern the I antigen formation.
Conclusion
In this K-562 cell model when induced by SB, the SHP-2-ERK2 signaling is specific for the branched poly-LacNAc formation during erythroid-differentiation.
Session topic: E-poster
Keyword(s): C/EBP, ERK, Erythroid differentiation, SHP-2
Abstract: E1569
Type: Eposter Presentation
Background
The straight and branched repeats of poly-LacNAc chains characterize the histo-blood group i and I antigens, respectively. In the human hematopoietic cell model, the transcription factor CCAAT/enhancer binding protein a (C/EBPa) regulates branched I antigen formation through IGnTC expression in both erythroid- and granulocytic-differentiation. However, the detail mechanisms for the regulation on the I synthesis along these different lineages remain unclear.
Aims
To investigate the regulatory mechanisms for branched I antigen formation during the erythroid- and granulocytic-differentiation.
Methods
The sodium butyrate (SB)- and retinoic acid (RA)-induced differentiated K-562 cells were served as the erythroid- and granulocytic-differentiation model, respectively. The wild type and mutant form of ERK2 and SHP-2-overexpressing K-562 cells were used to study the involvement of MAP kinase-mediated pathways and upstream signaling molecule in the I antigen formation. CHIP analysis was used to compare the binding affinity of C/EBPa to IGnTC promoter.
Results
The ERK2-mediated signaling specifically regulated the synthesis of I antigens during the erythroid-differentiation, but not for granulocytic-differentiation. SHP-2 acted as upstream regulator of ERK2 to control the phosphorylation status of Ser21 on C/EBPa, which affect the binding affinity to IGnTC regulatory region, and to govern the I antigen formation.
Conclusion
In this K-562 cell model when induced by SB, the SHP-2-ERK2 signaling is specific for the branched poly-LacNAc formation during erythroid-differentiation.
Session topic: E-poster
Keyword(s): C/EBP, ERK, Erythroid differentiation, SHP-2
Type: Eposter Presentation
Background
The straight and branched repeats of poly-LacNAc chains characterize the histo-blood group i and I antigens, respectively. In the human hematopoietic cell model, the transcription factor CCAAT/enhancer binding protein a (C/EBPa) regulates branched I antigen formation through IGnTC expression in both erythroid- and granulocytic-differentiation. However, the detail mechanisms for the regulation on the I synthesis along these different lineages remain unclear.
Aims
To investigate the regulatory mechanisms for branched I antigen formation during the erythroid- and granulocytic-differentiation.
Methods
The sodium butyrate (SB)- and retinoic acid (RA)-induced differentiated K-562 cells were served as the erythroid- and granulocytic-differentiation model, respectively. The wild type and mutant form of ERK2 and SHP-2-overexpressing K-562 cells were used to study the involvement of MAP kinase-mediated pathways and upstream signaling molecule in the I antigen formation. CHIP analysis was used to compare the binding affinity of C/EBPa to IGnTC promoter.
Results
The ERK2-mediated signaling specifically regulated the synthesis of I antigens during the erythroid-differentiation, but not for granulocytic-differentiation. SHP-2 acted as upstream regulator of ERK2 to control the phosphorylation status of Ser21 on C/EBPa, which affect the binding affinity to IGnTC regulatory region, and to govern the I antigen formation.
Conclusion
In this K-562 cell model when induced by SB, the SHP-2-ERK2 signaling is specific for the branched poly-LacNAc formation during erythroid-differentiation.
Session topic: E-poster
Keyword(s): C/EBP, ERK, Erythroid differentiation, SHP-2
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