Aperçu des produits pour anti-TLE1 (TLE1) Anticorps

Human Transducin-Like Enhancer of Split 1 (E(sp1) Homolog, Drosophila) (TLE1) interaction partners

1. Nuclear TLE1 expression was identified in 24 (57%) of the 42 melanoma cases with spindle cell morphology. TLE1 frequently highlights melanomas with spindle cell morphology and is a potential diagnostic pitfall. When evaluating spindle cell tumors in which the differential may include both a melanoma and synovial sarcoma, TLE1 expression should be interpreted with caution.

2. These results provide previously unavailable insight into the transcriptional programs underlying the tumour-promoting functions of FOXG1:TLE1 in glioblastoma.

3. These data are of particular interest and give support for a plausible role of TLE1 as a tumor suppressor in T-cell ALL. Moreover, the prognostic value of this corepressor may assist ALL treatment stratification and suggest the need of alternative regimens.

4. There is frequent expression of TLE1 in cutaneous neoplasms, including sebaceous neoplasms, basal cell carcinoma, and squamous cell carcinomas.

5. Using trio-based exome sequencing, we identified a homozygous missense mutation in the Transducin-like enhancer of split-1 (TLE1) gene, encoding for a non DNA-binding transcriptional corepressor, highly expressed in the postnatal brain

6. Case Report: primary subcutaneous biphasic synovial sarcoma with TlE1 immunoreactivity.

7. The majority of malignant rhabdoid tumors and atypical teratoid/rhabdoid tumor cases showed some TLE1 immunoreactivity (n = 16; 89% for >/=1 + staining); 14 (78%) of total cases showed >/=2 + positivity using any of the 3 scoring systems. Over half (n = 10; 56%) of cases showed >/=2 + staining; 4 (22%) cases showed 3 + strong and diffuse TLE1 staining measured by all scoring systems in agreement.

8. Immunohistochemical analysis for TLE1 can identify basal cell adenomas and basal cell adenocarcinomas by luminal cell staining difference, especially indistinct luminal cell expression for TLE1 in invasive areas of BCAC.

9. TLE1 is a potential immunohistochemical marker for glomus tumors

10. studies indicate Bit1 is an inhibitor of EMT and metastasis in lung cancer and hence can serve as a molecular target in curbing lung cancer aggressiveness

11. Authors present data indicating that TLE1 is rapidly excluded from the nucleus following epidermal growth factor receptor pathway activation, an effect that likely accounts for its inability to mediate effective repression under such conditions.

12. TLE1 is not a stand-alone diagnostic immunohistochemical marker for synovial sarcoma

13. Data suggest TLE1 is highly expressed in macrophages cultured in vitro, in macrophages of atherosclerotic plaques, and in macrophages of visceral adipose tissue from obese women; expression of TLE1 is up-regulated upon macrophage activation.

14. TLE1 has a role in regulating epithelial-to-mesenchymal transition in A549 cells through its repressive effect on E-cadherin

15. There was no difference in TLE-1 staining between different subtypes of synovial sarcoma

16. GrG1 is involved in pancreatic cell differentiation, establishing a monohormonal beta cell identity. Grg1 is the predominant Groucho expressed in human beta-cells but acts functionally similarly to Grg3.

17. TCF/TLE tetramer complex promotes structural transitions of chromatin to mediate repression.

18. highly specific biomarker for synovial sarcoma

19. signaling and increases the expression of recombinant recognition sequence binding protein at the Jkappa site (RBP-J) and transducin-like enhancer of Split (TLE).

20. Although molecular confirmation is the diagnostic gold standard for synovial sarcoma, TLE1, in view of its high sensitivity may be a useful marker within the optimal IHC panel comprising EMA, BCL2, MIC2, CD34 and CK7

Mouse (Murine) Transducin-Like Enhancer of Split 1 (E(sp1) Homolog, Drosophila) (TLE1) interaction partners

1. These findings indicate that Tle corepressors are differentially partitioned to Runx and Tcf/Lef complexes to instruct CD8(+) lineage choice and cooperatively establish CD8(+) T cell identity, respectively.

2. Demethylation of TLE1 promoter region activates the self-expression in diabetic mice intestinal epithelium cells (IECs). Subsequently, TLE1, through the transcriptional suppression on expression of Hes1, contributes to the aberrant differentiation of IECs in DM mice.

3. Data suggest that Tle1 is highly expressed in activated macrophages cultured in vitro; expression of Tle1 is low in resting macrophages and is up-regulated upon macrophage activation (here, stimulated with recombinant human interleukin-4).

4. Loss of Tle1 not only results in increased phosphorylation and activation of proinflammatory NF-kappaB but also results in decreased Hes1 (hairy and enhancer of split-1), a negative regulator of inflammation in macrophages

5. TLE1/TLE3-NuRD corepressor complex facilitates Tbx20-dependent transcriptional repression.

6. Data indicate that cAMP activates Notch signaling and increases the expression of recombinant recognition sequence binding protein at the Jkappa site (RBP-J) and transducin-like enhancer of Split (TLE).

7. TLE is important to promote the formation of the p3 domain and subsequent generation of V3 interneurons.

8. Studies suggest that TLE1 and TLE3 might also play roles independent of HESX1 by interacting with other transcription factors like PROP1.

9. Grg1-S may operate in conjunction with beta-catenin and Tcf factors to regulate vertebrate gut epithelial cell differentiation

10. Grg6 interferes with the binding of Gro/TLE1 to BF-1 and does not repress transcription when targeted to DNA.

11. Inhibition of cortical neuron differentiation by Groucho/TLE1 requires interaction with WRPW, but not Eh1, repressor peptides