anti-delta-Like 1 Homolog (Drosophila) (DLK1) Anticorps

Cow (Bovine) delta-Like 1 Homolog (Drosophila) (DLK1) interaction partners

1. DLK1 mRNA expression in mesenteric fat was higher than subcutaneous fat. DLK1 mRNA expression in Holstein cattle mesenteric fat was higher than Wagyu cattle.

2. The four loci of DLK1 gene and CLPG gene in 1109 individuals, which belong to eight breeds/species of bovidae, including cattle, buffalo and yak, were analyzed.

3. tissue-specific expression patterns of Dlk-1 splice variants in bovine tissues

Human delta-Like 1 Homolog (Drosophila) (DLK1) interaction partners

1. point mutations in DLK1 and KCNK9 (Montrer KCNK9 Anticorps) at least do not seem to be a common cause of central precocious puberty in girls.

2. The expression of piRNAs encoded at DLK1-DIO3 (Montrer DIO3 Anticorps) enhances the prognostic potential of small non-coding RNAs specific to this locus in predicting lung cancer patient outcome.

3. targeting DLK1 might inhibit the tumor growth via initiating cell differentiation of hepatocellular carcinoma (HCC (Montrer FAM126A Anticorps)) cancer stem cell.

4. SASH1 (Montrer SASH1 Anticorps) acts through NOTCH1 (Montrer NOTCH1 Anticorps) and its inhibitor DLK1 in a three-dimensional model of lumenogenesis involving CEACAM1 (Montrer CEACAM1 Anticorps).

5. The data presented in this work suggest that a fine regulation of NOTCH (Montrer NOTCH1 Anticorps) signaling BY DLK1 plays an important role in the control of breast cancer cell proliferation and invasion.

6. results demonstrate that miR (Montrer MLXIP Anticorps)-129-5p inhibits non-small cell lung cancer stemness and chemoresistance through direct targeting of DLK1

7. A complex defect of DLK1 ( approximately 14-kb deletion and 269-bp duplication) was identified in a family with central precocious puberty. This deletion included the 5' untranslated region and the first exon of DLK1, including the translational start site. Only family members who inherited the defect from their father have precocious puberty, consistent with the known imprinting of DLK1.

8. Loss of DLK1 expression is associated with fetal growth retardation complications of pregnancy.

9. In neonatal skin, DLK1 exhibited a high degree of monoallelic expression from the paternal allele.

10. The study evaluated the roles of extracellular soluble DLK1, comprising six EGF (Montrer EGF Anticorps)-like domains and juxtamembrane regions, in human pancreatic cancer MIA (Montrer MIA Anticorps) PaCa-2 cells in vitro and in vivo. Soluble DLK1 exerted antitumor effects not only in cancer cell migration and anchorage-independent cell growth but also in in vivo tumor growth.

Pig (Porcine) delta-Like 1 Homolog (Drosophila) (DLK1) interaction partners

1. trans-associations occur between three imprinted genes IGF2, DLK1 and MEG3 both in fetal liver and muscle cells.

2. We did not observe significantly different expression of DLK1, MEG3 or PEG11 (Montrer RTL1 Anticorps) mRNA in any of analyzed breeds.

3. QUASEP supports paternal expression of DLK1 in whole brain, carcass, liver and placental tissues of day 30 interbreed porcine fetuses.

4. the sequence of porcine DLK1 (pDLK1)was examined,the expression and alternative splicing isoforms in the pig (Sus scrofa) was compared with human

5. Polymorphisms, imprinting status and quantitative trait locus analyses of the porcine DLK1 and MEG3 genes i swine.

6. Expression of DLK1 splice variants during adipocyte development in vitro and in vivo.

Mouse (Murine) delta-Like 1 Homolog (Drosophila) (DLK1) interaction partners

1. Functional analysis revealed that ground-state miRNAs embedded in the Dlk1-Dio3 (Montrer DIO3 Anticorps) locus (miR (Montrer MLXIP Anticorps)-541-5p, miR (Montrer MLXIP Anticorps)-410-3p, and miR (Montrer MLXIP Anticorps)-381-3p) promoted pluripotency via inhibition of multi-lineage differentiation and stimulation of self-renewal

2. This study suggests that Pref-1 is an endocrine factor which is synergistically increased by obesity and age.

3. Gene body methylation of noncoding RNA genes was observed and among these microRNA genes were prominent. Of particular note, observed only in hyperphenylalaninemic animals, was hypomethylation of miRNA genes within the imprinted Dlk1-Dio3 (Montrer DIO3 Anticorps) locus on chromosome 12.

4. The role of elevated oxygen levels in eroding imprinted Dlk1 expression during prolonged culture and in vitro differentiation.

5. Loss of DLK1 expression is associated with fetal growth retardation complications of pregnancy.

6. Pref-1 mRNA is a novel substrate of RNase-L (Montrer RNASEL Anticorps).

7. the conserved sequences in IG-DMR (Montrer WDR20 Anticorps) are involved in the expression regulation of some of the imprinted genes in the Dlk1-Dio3 (Montrer DIO3 Anticorps) domain

8. To investigate the nature of these more variably methylated secondary differentially methylated regions, we adopted a hairpin linker bisulfite mutagenesis approach to examine CpG dyad methylation at differentially methylated regions associated with the murine Dlk1/Gtl2 imprinting cluster on both complementary strands.

9. NOTCH1 (Montrer NOTCH1 Anticorps) ligand Delta-like 1 (Montrer DLL1 Anticorps) homolog (DLK1) self interacts

10. the salivary gland phenotype of Dlk1 knock-out mice, was investigated.