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Left-right determination factor 2

lefty2, EBAF, endometrial bleeding associated factor
This gene encodes a member of the TGF-beta family of proteins. The encoded protein is secreted and plays a role in left-right asymmetry determination of organ systems during development. The protein may also play a role in endometrial bleeding. Mutations in this gene have been associated with left-right axis malformations, particularly in the heart and lungs. Some types of infertility have been associated with dysregulated expression of this gene in the endometrium. Alternative processing of this protein can yield three different products. This gene is closely linked to both a related family member and a related pseudogene. Alternate splicing of this gene results in multiple transcript variants. [provided by RefSeq, Feb 2010] (from NCBI)
Top mentioned proteins: Lefty1, NODAL, RGS, TGF-beta, Midline
Papers on lefty2
Microarray Analyses Reveal Marked Differences in Growth Factor and Receptor Expression Between 8-Cell Human Embryos and Pluripotent Stem Cells.
Kiessling et al., Athens, Greece. In Stem Cells Dev, Feb 2016
Forty-four gene elements were underdetected on the 8C arrays, including 11 at least 80-fold under the pluripotent cells: two cytokines (IFITM1, TNFRSF8), five TGFBs (BMP7, LEFTY1, LEFTY2, TDGF1, TDGF3), two FGFs (FGF2, FGF receptor 1), plus ING5, and WNT6.
Heightened potency of human pluripotent stem cell lines created by transient BMP4 exposure.
Roberts et al., Columbia, United States. In Proc Natl Acad Sci U S A, Jun 2015
The cells have a distinct transcriptome profile from the human PSCs from which they were derived (including higher expression of NANOG, LEFTY1, and LEFTY2).
Cross platform analysis of methylation, miRNA and stem cell gene expression data in germ cell tumors highlights characteristic differences by tumor histology.
Tolar et al., Minneapolis, United States. In Bmc Cancer, 2014
Using the MIC, we identified correlations across the data features, including six major hubs with higher expression in YST (LEFTY1, LEFTY2, miR302b, miR302a, miR 126, and miR 122) compared with other GCT.
Gene expression profiling of somatic and pluripotent cells reveals novel pathways involved in reprogramming.
Dai et al., Guangzhou, China. In Genet Mol Res, 2014
Several genes with the expression levels that were significantly different between ES and iPS cells were found, including LEFTY2, DLK1, and NLRP2.
Exploratory genotype-phenotype correlations of facial form and asymmetry in unaffected relatives of children with non-syndromic cleft lip and/or palate.
Moreno Uribe et al., Iowa City, United States. In J Anat, 2014
Cases and controls were genotyped for 20 SNPs across 13 candidate genes for NSCL/P (PAX7, ABCA4-ARHGAP29, IRF6, MSX1, PITX2, 8q24, FOXE1, TGFB3 and MAFB) and left-right body patterning (LEFTY1, LEFTY2, ISL1 and SNAI1).
FGF signaling is required for brain left-right asymmetry and brain midline formation.
Yost et al., Salt Lake City, United States. In Dev Biol, 2014
When FGF signaling is inhibited during mid-somitogenesis, asymmetrically expressed LPM markers southpaw and lefty2 are not affected.
Orphan G-protein coupled receptor 22 (Gpr22) regulates cilia length and structure in the zebrafish Kupffer's vesicle.
Tylzanowski et al., Leuven, Belgium. In Plos One, 2013
Specifically, defective LR patterning included randomization of the left-specific lateral plate mesodermal genes (LPM) (lefty1, lefty2, southpaw and pitx2a), resulting in randomized cardiac looping.
Differential diffusivity of Nodal and Lefty underlies a reaction-diffusion patterning system.
Schier et al., Cambridge, United States. In Science, 2012
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
LEFTY2 expression and localization in rat oviduct during early pregnancy.
Miceli et al., San Miguel de Tucumán, Argentina. In Zygote, 2012
LEFTY2 is expressed at a high level just before the embryos pass to the uterus; its biological effect might be relevant and significant for the preimplantation stage of embryo development in the oviduct.
The Nodal inhibitor Lefty is negatively modulated by the microRNA miR-302 in human embryonic stem cells.
Menendez et al., Armilla, Spain. In Faseb J, 2011
Findings suggest that Lefty2 is negatively modulated by miR-302s in hESCs, which plays an important role in maintaining the balance between pluripotency and germ layer specification.
Isolation, characterization, and function of EBAF/LEFTY B: role in infertility.
Tabibzadeh, Stony Brook, United States. In Ann N Y Acad Sci, 2011
Findings show that during embryonic development, EBAF/LEFTY B plays important roles in decidualization and embryo implantation.
Target protectors reveal dampening and balancing of Nodal agonist and antagonist by miR-430.
Schier et al., Cambridge, United States. In Science, 2007
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
Cited2 controls left-right patterning and heart development through a Nodal-Pitx2c pathway.
Bhattacharya et al., Oxford, United Kingdom. In Nat Genet, 2004
Cited2(-/-) mice lack expression of the Nodal target genes Pitx2c, Nodal and Ebaf in the left lateral plate mesoderm, where they are required for establishing laterality and cardiovascular development.
Molecular genetic analysis of left-right handedness in plants.
Hashimoto, Ikoma, Japan. In Philos Trans R Soc Lond B Biol Sci, 2002
Recessive spiral1 and spiral2 mutants show right-handed helical growth in roots, hypocotyls, petioles and petals; semi-dominant lefty1 and lefty2 mutants show opposite left-handed growth in these organs.
Asymmetry: molecular, biologic, embryopathic, and clinical perspectives.
Cohen, Halifax, Canada. In Am J Med Genet, 2001
This overview of asymmetry addresses the following topics: chiral molecules; asymmetric signaling molecules, including N-cadherin, Shh, Fgf8, lefty1, lefty2, nodal, Pitx2, activin betaB, activin receptor IIA, and cSnR; situs abnormalities; asymmetric cell division; laterality in humans and animals; behavioral asymmetry in humans and animals; asymmetric embryopathies, including Tessier-type "clefts"; hemiasymmetries such as hemihyperplasia, hemihypoplasia, and hemiatrophy; asymmetric vascular syndromes, including Klippel-Trenaunay and Sturge-Weber syndromes; plagiocephaly of the synostotic and deformational types; somatic mosaicism, including a discussion of McCune-Albright syndrome, fibrous dysplasia, GNAS1 mutations, and Proteus syndrome.
Establishment of left-right asymmetry.
Yost, Salt Lake City, United States. In Int Rev Cytol, 2000
These mechanisms appear to converge on highly conserved expression patterns of genes in the transforming growth factor-beta (TGFbeta) family of cell-cell signaling factors, nodal and lefty-2, and subsequently the expression of the transcription regulator Pitx2, in left lateral plate mesoderm.
Loss-of-function mutations in the EGF-CFC gene CFC1 are associated with human left-right laterality defects.
Casey et al., Bethesda, United States. In Nat Genet, 2000
5), LEFTB (formerly LEFTY2; ref. 6) and ACVR2B (encoding activin receptor IIB; ref. 7).
Regulation of left-right patterning in mice by growth/differentiation factor-1.
Lee et al., Baltimore, United States. In Nat Genet, 2000
In most Gdf1-/- embryos, the expression of Ebaf (formerly lefty-1) in the left side of the floor plate and Leftb (formerly lefty-2), nodal and Pitx2 in the left lateral plate mesoderm was absent, suggesting that Gdf1 acts upstream of these genes either directly or indirectly to activate their expression.
The SIL gene is required for mouse embryonic axial development and left-right specification.
Kuehn et al., Bethesda, United States. In Nature, 1999
Comparison with Shh mutant embryos, which have axial defects but normal cardiac looping, indicates that the consequences of abnormal midline development for left-right patterning depend on the time of onset, duration and severity of disruption of the normal asymmetric patterns of expression of nodal, lefty-2 and Pitx2.
Randomization of left-right asymmetry due to loss of nodal cilia generating leftward flow of extraembryonic fluid in mice lacking KIF3B motor protein.
Hirokawa et al., Tokyo, Japan. In Cell, 1999
lefty-2 expression was either bilateral or absent.
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