Dec 25, 2024 · TSPAN32 (Tetraspanin 32) is a Protein Coding gene. Diseases associated with TSPAN32 include Beckwith-Wiedemann Syndrome and Myeloma, Multiple. An important paralog of this gene is TSPAN2. May be produced at very low levels due to a premature stop codon in the mRNA, leading to nonsense-mediated mRNA decay. Belongs to the tetraspanin (TM4SF) family.

Mar 1, 2023 · We found that TSPAN32 expression was repressed by BCR-ABL and ectopic TSPAN32 expression upon Imatinib treatment inhibited the proliferation of Ph + cell lines. Tspan32 overexpression...

Tetraspanin-32 is a protein that in humans is encoded by the TSPAN32 gene. [5][6][7] This gene is described as a member of the tetraspanin superfamily whose expression is confined to hematopoietic tissues. [7]

This gene, which is a member of the tetraspanin superfamily, is one of several tumor-suppressing subtransferable fragments located in the imprinted gene domain of chromosome 11p15.5, an important tumor-suppressor gene region.

Jan 11, 2025 · In this study, we performed a comprehensive analysis of the expression patterns and regulatory roles of TSPAN32. Notably, TSPAN32 is highly expressed in immune cells, particularly in natural killer (NK) cells and CD8+ T cells.

Mar 1, 2023 · Tspan32 overexpression significantly prevented BCR-ABL induced leukemia progression in a murine model and impaired leukemia stem cell (LSC) proliferation. LSCs represent an obstacle for chronic myeloid leukemia (CML) elimination, which continually replenish leukemia cells and are associated with disease relapse.

我们在此报告， tspan32是费城 (ph + ) 白血病发病机制的关键节点因子。我们发现tspan32表达被 bcr-abl 抑制，并且伊马替尼治疗后异位 tspan32 表达抑制 ph +细胞系的增殖。 tspan32过表达可显着阻止 bcr-abl 在小鼠模型中诱导的白血病进展，并损害白血病干细胞 (lsc) 增殖。

Apr 22, 2024 · However, Tspan32 stands as a notable exception to the overall pro-tumorigenic role of Tspans. Its overexpression effectively impedes leukemia progression and impairs the proliferation of leukemia...

Here, we show that TSPAN32 is expressed at higher levels in the lymphoid lineage as compared to myeloid cells. In vitro activation of T helper cells via anti-CD3/CD28 is associated with a significant downregulation of TSPAN32.

The present study focuses on the characterization of TSPAN32 in T cell responses and provides the first proof of concept for a possible role of TSPAN32 in the immune dysregulation observed in MS, defining this molecule as a potential translational target for further studies.