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Wenbin Wang

Publications and source records attributed to Wenbin Wang.

5 recordsLinked to original sources

Overexpression of the tomato SlLEA_2-26 gene enhances the tolerance to drought and salt stresses in Arabidopsis thaliana.

Late embryogenesis abundant (LEA) proteins are pivotal in conferring cellular tolerance to abiotic stresses and sustaining plant growth and development. However, systematic functional characterization of the tomato SlLEA_2 gene family remains limited. To elucidate the role of tomato SlLEA_2-26 in abiotic stress responses, this study cloned its full-length cDNA. Quantitative real-time PCR (qRT-PCR) analysis revealed that SlLEA_2-26 exhibits predominant expression in flowers and fruits, and is strongly induced by drought, salt, Cu2+, and Pb2+ stresses. Three homozygous Arabidopsis thaliana T3 SlLEA_2-26-overexpression lines were generated and confirmed via genomic PCR. Under drought and salt stress, T3 A. thaliana lines overexpressing SlLEA_2-26 exhibited significantly enhanced seed germination rates, root elongation, and fresh weights compared to wild type (WT) plants, indicating improved stress tolerance during early seedling development. Furthermore, transgenic plants accumulated higher levels of soluble sugar and proline, and displayed elevated antioxidant enzyme activity compared to the WT, whereas contents of malondialdehyde (MDA) and reactive oxygen species (ROS) were markedly reduced relative to WT. qRT-PCR analysis confirmed the significant upregulation of SlLEA_2-26 in transgenic lines under drought and salt stress conditions, accompanied by elevated expression of AtP5CS1, AtCSD1, AtRD29A, AtRD26, and AtNCED3. Collectively, these results demonstrate that SlLEA_2-26 overexpression enhances drought and salt stress tolerance in A. thaliana by promoting the accumulation of osmoregulatory substances, augmenting antioxidant defense capacity, and activating stress-responsive gene expression. This study provides a theoretical foundation and valuable genetic resources for breeding stress-tolerant tomatoes and other crops.

SlLEA_2–26↗

Systematic decoding of functional enhancer connectomes and risk variants in human glioma.

Genetic and epigenetic variations contribute to the progression of glioma, but the mechanisms underlying these effects, particularly for enhancer-associated genetic variations in non-coding regions, still remain unclear. Here we performed high-throughput CRISPR interference screening to identify pro-tumour enhancers in glioma cells. By integrating genome-wide H3K27ac HiChIP data, we identified the target genes of these pro-tumour enhancers and revealed the essential role of enhancer connectomes in promoting glioma progression. Through systematic analysis of enhancers carrying glioma risk-associated single-nucleotide polymorphisms (SNPs), we found that these SNPs can promote glioma progression through the enhancer connectome. Using CRISPR-Cas9-mediated enhancer interference and SNP editing, we demonstrated that glioma-specific enhancer carrying the risk SNP rs2297440 regulates SOX18 expression by specifically recruiting transcription factor MEIS1 binding, thereby contributing to glioma progression. Our study sheds light on the molecular mechanisms underlying glioma susceptibility and provides potential therapeutic targets to treat glioma.

Humans↗

[Inherited dysfibrinogenemia caused by Arg275His in the beta chain of fibrinogen].

OBJECTIVE: To analyze the phenotype and genotype of a family with inherited dysfibrinogenemia. METHODS: Laboratory tests including activated particle thromboplastin time (APTT), prothrombin time (PT), thrombin time (TT), and the activity of protein C (PC), protein S(PS) and antithrombin (AT) were conducted in the proband and 4 family members. The activity and antigen of fibrinogen in plasma were measured by functional and immunoturbidimetry assay, respectively. All the exons and exon-intron boundaries of the three fibrinogen genes were analyzed by direct sequencing. RESULTS: The proband had normal APTT and PT, but prolonged TT. Her plasma fibrinogen levels were extremely reduced, which was also found in her mother. The sequencing results of the proband revealed heterozygous g.5678 G>A in the exon 8 of FGG gene originating from her mother, which caused Arg275His missense mutation. CONCLUSION: Dysfibrinogenemia in the family is caused by Arg275His in the beta chain of fibrinogen and it is the first report on a Chinese family with inherited dysfibrinogenemia.

Adult↗

[A new ST segment analysis scheme for Holter system].

A new ST segment analysis scheme is developed for helping the doctors to browse the electrocardiogram (ECG) signals rapidly and then give a correct diagnosis. The preprocessing consists of baseline wander attenuation using median filter, high frequency noise rejection using order statistic filter, and then QRS complexes detection using wavelet analysis. In this paper, after the beginnings and the ends of the ST segments are mutually chosen by doctor, we compute the total deviations between ST segments and the modified baselines using mean value, and then plot the whole trend of the deviations. Doctors can browse the original ECG signals handily by our browsing system, and then give a diagnosis colligating other clinic features of the patient.

Electrocardiography, Ambulatory↗