anti-Left-Right Determination Factor 1 (LEFTY1) Antibodies

Zebrafish Left-Right Determination Factor 1 (LEFTY1) interaction partners

1. Theauthors find that zebrafish lefty mutants exhibit excess Nodal signaling and increased specification of mesendoderm, resulting in embryonic lethality.

2. Our data do not support the reaction-diffusion model, but instead, we propose that Nodal activates signaling in a temporal window that is defined by a miR-430-mediated delay of Lft1/2 translation

3. results indicate that differential diffusivity is the major determinant of the differences in Nodal/Lefty range and provide biophysical support for reaction-diffusion models of activator/inhibitor-mediated patterning

4. both Nodal and Bmp independently are required for lefty1 expression to assure unilateral Nodal activation and correct LR patterning

5. Bmp represses Nodal signaling independently of lefty1 expression and through the activity of a ligand other than Bmp4.

6. we find that Cyclops is specifically required for the maintenance of lefty1 and lefty2 transcription

7. study reports that microRNA-430 (miR-430) dampens and balances the expression of the transforming growth factor-beta (TGF-beta) Nodal agonist squint and the TGF-beta Nodal antagonist lefty

Mouse (Murine) Left-Right Determination Factor 1 (LEFTY1) interaction partners

1. A cell that experiences the highest level of Nodal signaling begins to express Lefty1 and becomes an L1(epi) cell. Deletion of Lefty1 alone or together with Lefty2 increased the number of prospective DVE cells

2. Lefty1 may ameliorate renal tubulointerstitial inflammation by suppressing NFkappaB signaling.

3. results show that TET-mediated oxidation of 5-methylcytosine modulates Lefty-Nodal signalling by promoting demethylation in opposition to methylation by DNMT3A and DNMT3B; findings reveal a fundamental epigenetic mechanism featuring dynamic DNA methylation and demethylation crucial to regulation of key signalling pathways in early body plan formation

4. exogenous lefty1 administered to mice restored the endogenous expression levels of lefty1. The present study demonstrated that lefty1 attenuated renal interstitial injury by inhibiting the Smaddependent TGFb1 signaling pathway

5. Lefty-1 may prevent TGFB1-induced fibroblast-myofibroblast transdifferentiation in part via modulation of Smad3, JNK-3, and BMP-5 signaling.

6. The expression of lefty in RCC cells was lower than that in adjacent non-tumor cells, which may result in the overexpression of nodal, thereby promoting the growth of RCC.

7. Studies indicate that the pair of Nodal and Lefty (Lefty1 and Lefty2) has a conserved role in left-right asymmetry.

8. Taken together, these results suggest that optimal expression of Lefty1 and Lefty2 is critical for the balanced differentiation of mESCs into three germ layers.

9. Beta-catenin can recruit the H3K4me2/1 demethylase LSD1 to regulate the expression of the tumor suppressor Lefty1 in mouse embryonic stem cells.

10. Lefty can antagonise TGF-beta1 mediated epithelial-mesenchymal transition in renal tubular epithelial cells.

11. modulates both the induction of decidual differentiation and the maintenance of a decidualized state by an autocrine mechanism

12. Cerberus-like and Lefty-1 function redundantly to modulate Nodal signaling during gastrulation and regulate patterning of the primitive streak

13. Regulated expression and spatial distribution of lefty in mouse endometrium confines its biological impact on tissues that undergo remodelling during estrous cycle and pregnancy.

14. findings show that decidualized differentiation of stroma, which is a prerequisite for embryo implantation, leads to processing of lefty by PC5/6A

15. The gene for Lefty1 protein, a Nodal antagonist that influences the direction of DVE migration, was found to be asymmetrically expressed in the primitive endoderm of the implanting blastocyst.

16. after stimulation, the protease activity of PC5A is enhanced, as evidenced by the cleavage of the PC5A substrates Lefty, ADAMTS-4, endothelial lipase, and PCSK9.

17. Data suggest that Nodal and lefty signaling regulates the growth of pancreatic cells.

Human Left-Right Determination Factor 1 (LEFTY1) interaction partners

1. functional role of LEFTY during progesterone therapy for endometrial carcinoma

2. Studied genes involved in TGF-beta/BMP signaling pathway including chorionic villi LEFTY1 expression levels in association with miscarriage.

3. Lefty1 could regulates the cell cycle via modulating the expressions of P57 and cyclin D1 and then inhibit the decidualization in vitro.

4. The mRNA levels of LSD1 and beta-catenin are inversely correlated with the levels of Lefty1 in pancreas and breast tumors.

5. Reprogrammed cancer cells share the mechanism for expression of Lefty with induced pluripotent cancer cells (iPS), thus contributing to the cancerous transformation of iPS cells.

6. Data suggest that Lefty is a novel TGF-beta target molecule that mediates growth inhibition of pancreatic cancer cells.

7. Findings suggest that Lefty1 is negatively modulated by miR-302s in hESCs, which plays an important role in maintaining the balance between pluripotency and germ layer specification.

8. Findings show that during embryonic development, EBAF/LEFTY B plays important roles in decidualization and embryo implantation.

9. The expression of Nodal in normal and malignant endometrial cells that lack Lefty strongly supports an important role for this embryonic morphogen in the tissue remodelling events that occur across the menstrual cycle and in tumourogenesis.

10. nodal and the inhibitors of Nodal signaling, lefty-A and lefty-B, are down-regulated very early upon differentiation of human embryonic stem cells

11. LEFTY proteins, which are known to play a major role during mouse gastrulation, are transiently expressed during human embryonic stem cell differentiation.