TCF3 / E2A pThr355 antibody Ab
- Known as:
- TCF3 / E2A pThr355 (anti-) Antibody
- Catalog number:
- 1488254
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- TCF3 / E2A pThr355 antibody
Related genes to: TCF3 / E2A pThr355 antibody Ab
- Gene:
- TCF3 NIH gene
- Name:
- transcription factor 3
- Previous symbol:
- -
- Synonyms:
- E2A, ITF1, MGC129647, MGC129648, bHLHb21, VDIR, E47, p75
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-07-26
- Date modifiied:
- 2019-04-23
- Gene:
- TCF7L1 NIH gene
- Name:
- transcription factor 7 like 1
- Previous symbol:
- TCF3
- Synonyms:
- -
- Chromosome:
- 2p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-01-20
- Date modifiied:
- 2016-02-01
Related products to: TCF3 / E2A pThr355 antibody Ab
Related articles to: TCF3 / E2A pThr355 antibody Ab
- Early B cell lymphopoiesis depends on E2A, Ebf1, Pax5 and Ikaros family members. In the present study, we used acute protein degradation in mice to identify direct target genes of these transcription factors in pro-B, small pre-B and immature B cells. E2A, Ebf1 and Pax5 predominantly function as transcriptional activators by inducing open chromatin at their target genes, have largely unique functions and are essential for early B cell maintenance. Ikaros and Aiolos act as dedicated repressors to cooperatively control early B cell development. The surrogate light-chain genes Igll1 and Vpreb1 are directly activated by Ebf1 and Pax5 in pro-B cells and directly repressed by Ikaros and Aiolos in small pre-B cells. Pax5 and E2A contribute to V(D)J recombination by activating Rag1, Rag2, Dntt, Irf4 and Irf8. Similar to Pax5, Ebf1 also represses the cohesin-release factor gene Wapl to mediate prolonged loop extrusion across the Igh locus. In summary, in vivo protein degradation has provided unprecedented insight into the control of early B cell lymphopoiesis by five transcription factors. - Source: PubMed
Publication date: 2024/08/23
Fedl Anna STagoh HiromiGruenbacher SarahSun QiongSchenk Robyn LFroussios KimonJaritz MarkusBusslinger MeinradSchwickert Tanja A - Although there are many treatments for breast cancer, such as surgery, radiotherapy, chemotherapy, estrogen receptor antagonists, immune checkpoint inhibitors and so on. However, safer and more effective therapeutic drugs for breast cancer are needed. Sinensetin, a safer therapeutic drugs, come from citrus species and medicinal plants used in traditional medicine, while its role and underlying mechanism in breast cancer remain unclear. Our study aimed to investigate the role and mechanism of sinensetin in breast cancer. - Source: PubMed
Publication date: 2024/01/12
Zhu ShengqianMeng LifeiWei PengGu GuowenDuan Keli - ALK-negative anaplastic large cell lymphoma (ALCL) cases with 6p25.3 rearrangement are characterized by peculiar morphological and immunohistochemical features compare to 6p25.3-negative ALK-negative ALCL cases. A subgroup of 6p25.3-positive ALK-negative ALCL cases show the t(6,7) (p25.3;q32.3) rearrangement. Aims: To analyse the differences between 6p25.3-rearranged cases with and without t(6,7) (p25.3;q32.3). Using RNA-sequencing we studied a series of 17 samples showing 6p25.3-rearrangement, identified by FISH, consisting of seven systemic and eight primary cutaneous cases including two examples of secondary skin involvement by systemic ALCL. RNA-sequencing exclusively detected a translocation involving a gene in the 6p25.3 region (either IRF4 or DUSP22) in 7/14 cases (50%). In six of these seven cases the partner proved to be the LINC-PINT region in chromosome 7, while an EXOC2::DUSP22 rearrangement was found in one case. All cases but one were primary cutaneous ALCLs. They all were CD3 positive and BCL2 negative, while most of them expressed p-STAT3. On the contrary, cases without the t(6,7) (p25.3;q32.3) were mainly systemic (71%, 5/7) against just two pcALCL. In general, they lose CD3 (50% positive) and p-STAT3 (25% positive) expression, being all of them BCL2 positive. Moreover, in 60% of them other gene fusions were found. At the transcriptional level, they were characterized by the overexpression of TCF3 (TCF7L1/E2A), DLL3, CD58 and BCL2 genes 75%(6/8) of pcALCL with 6p25.3 rearrangement featured the so-called "biphasic morphologic pattern, which was not found in cutaneous involvement from systemic ALCL. 83% (5/6) of the pcALCL cases with the "biphasic morphologic pattern" showed the t(6,7) (p25.3;q32.3) rearrangement. ALK-negative ALCL cases with 6p25.3 rearrangement are a subgroup of tumours that are heterogeneous with respect to the presence or absence of the t(6,7) (p25.3;q32.3) translocation. - Source: PubMed
Publication date: 2023/04/29
Díaz de la Pinta Francisco JavierRodríguez Moreno MartaSalgado Rocío NievesCarvajal García NereaSantonja CarlosPérez Buira SandraPiris Miguel ARequena LuisManso RebecaRodríguez-Pinilla Socorro María - Recent studies have reported the promising value of differential gene expression analysis and weighted gene coexpression network analysis (WGCNA) for identifying disease biomarkers. Based on this method, this study intends to characterize the hub genes and pathways related to retinal photoreceptor cell (PRC) injury in the context of retinitis pigmentosa (RP). A total of 53 coexpression modules were identified by WGCNA, among which lightpink4, darkolivegreen, tan4, blue2, skyblue2, and navajowhite2 ranked at the top. By analyzing the RP microarrays retrieved from the GEO database, 338 differentially expressed genes (DEGs) were identified in the RP samples. Forty-five candidate genes were selected from these DEGs by intersection with the genes in the coexpression modules. These intersection genes were subjected to GO and KEGG analyses. Furthermore, the genes and pathways involved in PRC damage were identified based on analyses utilizing GeneCards and STRING tools. Transcription factor 7-like 1 (TCF7L1, also called TCF3) was suggested to participate in the RP-associated PRC damage through the Wnt signaling pathway. It was validated in a blue light-irradiated cell model that TCF7L1 overexpression boosted PRC viability and repressed apoptosis. Inhibition of the Wnt signaling pathway also contributed to protective effects. Together, the data mentioned above supported the conclusion that either elevation of TCF7L1 or blockade of the Wnt signaling pathway could prevent RP progression by protecting PRCs from damage. - Source: PubMed
Yin YuanWu ShuaiNiu LingzhiHuang Shiwei - Objective To investigate the expression of T cell factor 3 (TCF3) in hepatocellular carcinoma (HCC), its correlation with the prognosis of HCC patients, and its effect on the invasion, migration, and metastasis of HCC cells. Methods The expression of TCF3 mRNA in HCC tissues was detected with tumor public databases and the expression of TCF3 protein in HCC specimens was detected by immunohistochemical staining. Correlation between TCF3 expression and HCC patients' prognosis was analyzed. Western blot analysis was used to detect the expression of TCF3 in different human HCC cell lines, and lentivirus infection was conducted to construct TCF3-upregulated and TCF3-downregulated HCC cell lines. The effect of TCF3 on the invasion and migration of HCC cells was assessed by in vitro Transwell assay, and in vivo intrahepatic tumor implantation models were established to evaluate the effect of TCF3 on the metastatic capacity of HCC cells. Results The expression of TCF3 mRNA was significantly higher in HCC tissues than that in normal liver tissues, and high expression of TCF3 mRNA was closely correlated with decreased overall survival rates of HCC patients. In 120 cases of HCC tissues, the protein level of TCF3 was significantly higher than that in adjacent nontumor tissues, and patients with positive TCF3 expression had a markedly decreased overall survival rate and a higher recurrence rate compared with patients with negative TCF3 expression. In vitro Transwell assay indicated that TCF3 upregulation promoted the invasion and migration of PLC/PRF/5 cells, whereas knockdown of TCF3 inhibited the invasion and migration abilities of HCCLM3 cells. Intrahepatic tumor implantation models showed that TCF3 upregulation promoted the metastasis of PLC/PRF/5 cells, while TCF3 knockdown weakened the metastatic capacity of HCCLM3 cells. Conclusion TCF3 expression is significantly upregulated in human HCC tissues, and high TCF3 expression predicts a poor prognosis of HCC patients. TCF3 markedly promotes the invasion, migration, and metastasis of HCC cells. - Source: PubMed
Feng WeiboLiu YaoChen JieQiao ChenyangXia LiminWu Kaichun