Songxing Wang
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Songxing Wang has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
- Yun‐Ping Xu
Shenzhen Institution of Transfusion Medicine Shenzhen Blood Center Shenzhen China
5 shared publications S.‐Q. Gao
Immunogenetics Laboratory, Shenzhen Blood Center, Shenzhen, China
3 shared publicationsA.‐L. Yang
Immunogenetics Laboratory, Shenzhen Blood Center, Shenzhen, Guangdong, China
1 shared publication- Chengyao Li
Department of Transfusion Medicine, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, China
1 shared publication H.‐B. Zhang
Medical College of Shenzhen University, Shenzhen, China
1 shared publicationL.‐M. He
Immunogenetics Laboratory, Shenzhen Blood Center, Shenzhen, China
1 shared publication
Latest Publications
Association of HLA‐E single nucleotide polymorphisms with human myeloid leukemia
Single nucleotide polymorphisms (SNPs) of HLA‐E are related to the occurrence of many diseases, but their functions remain unclear. In this study, the function of SNPs at HLA‐E rs76971248 and rs1264457 on the myeloid leukemia cells was analyzed by a progressive procedure, included genotyping, mRNA transcription, regulatory element, protein expression, and anti‐tumor effect. The frequencies of rs76971248 G and rs1264457 G were found higher in myeloid leukemia patients than those in healthy blood donors (p < 0.05). For myeloid leukemia, rs76971248 T was protective, while rs1264457 G was susceptible. We also found that rs76971248 affected HLA‐E mRNA transcription and membrane HLA‐E (mHLA‐E) expression in K562 cells through differently binding to transcription factor HOXA5 (p < 0.0001), while rs1264457 affected mHLA‐E expression by changing mRNA transcription and an encoding amino acid (p < 0.01). In contrast, the expression of soluble HLA‐E (sHLA‐E) was not influenced by both rs1264457 and rs76971248. The higher HLA‐E expression was detected among myeloid leukemia patients, and the K562 cells with higher HLA‐E molecules played a significant inhibitory effect on the killing activity of NK‐92MI cells (p < 0.05). In conclusion, the higher HLA‐E expression of myeloid leukemia cells is promoted by rs76971248 G and rs1264457 G, which helps escape from NK‐92MI cells' killing.
Association of HLA‐E single nucleotide polymorphisms with human myeloid leukemia
Single nucleotide polymorphisms (SNPs) of HLA‐E are related to the occurrence of many diseases, but their functions remain unclear. In this study, the function of SNPs at HLA‐E rs76971248 and rs1264457 on the myeloid leukemia cells was analyzed by a progressive procedure, included genotyping, mRNA transcription, regulatory element, protein expression, and anti‐tumor effect. The frequencies of rs76971248 G and rs1264457 G were found higher in myeloid leukemia patients than those in healthy blood donors (p < 0.05). For myeloid leukemia, rs76971248 T was protective, while rs1264457 G was susceptible. We also found that rs76971248 affected HLA‐E mRNA transcription and membrane HLA‐E (mHLA‐E) expression in K562 cells through differently binding to transcription factor HOXA5 (p < 0.0001), while rs1264457 affected mHLA‐E expression by changing mRNA transcription and an encoding amino acid (p < 0.01). In contrast, the expression of soluble HLA‐E (sHLA‐E) was not influenced by both rs1264457 and rs76971248. The higher HLA‐E expression was detected among myeloid leukemia patients, and the K562 cells with higher HLA‐E molecules played a significant inhibitory effect on the killing activity of NK‐92MI cells (p < 0.05). In conclusion, the higher HLA‐E expression of myeloid leukemia cells is promoted by rs76971248 G and rs1264457 G, which helps escape from NK‐92MI cells' killing.
The novel KIR3DS1*083 allele identified in a southern Chinese Han individual
KIR3DS1*083 allele differs from the closest allele KIR3DS1*01301 by 3 mutations in exon 4.
The novel KIR3DS1*083 allele identified in a southern Chinese Han individual
KIR3DS1*083 allele differs from the closest allele KIR3DS1*01301 by 3 mutations in exon 4.
The novel KIR3DS1*084 allele identified in a southern Chinese Han individual
KIR3DS1*084 allele differs from the closest allele KIR3DS1*01301 at nucleotide 308 C>T in exon 3.
The novel KIR3DS1*084 allele identified in a southern Chinese Han individual
KIR3DS1*084 allele differs from the closest allele KIR3DS1*01301 at nucleotide 308 C>T in exon 3.
The novel KIR3DS1*085 allele identified in a southern Chinese Han individual
KIR3DS1*085 allele differs from the closest allele KIR3DS1*01301 at nucleotide 934 C>T in exon 5.
The novel KIR3DS1*085 allele identified in a southern Chinese Han individual
KIR3DS1*085 allele differs from the closest allele KIR3DS1*01301 at nucleotide 934 C>T in exon 5.
The novel KIR3DS1*082 allele identified in a southern Chinese Han individual
KIR3DS1*082 allele differs from the closest allele KIR3DS1*01301 at nucleotide 1114T>C in exon 8.
The novel KIR3DS1*082 allele identified in a southern Chinese Han individual
KIR3DS1*082 allele differs from the closest allele KIR3DS1*01301 at nucleotide 1114T>C in exon 8.
The novel KIR3DS1*078 allele identified in a southern Chinese Han individual
KIR3DS1*078 allele differs from the closest allele KIR3DS1*01301 at nucleotide 775 G>C in exon 5.
The novel KIR3DS1*078 allele identified in a southern Chinese Han individual
KIR3DS1*078 allele differs from the closest allele KIR3DS1*01301 at nucleotide 775 G>C in exon 5.