anti-Pleiomorphic Adenoma Gene-Like 1 (PLAGL1) Antibodies

Human Pleiomorphic Adenoma Gene-Like 1 (PLAGL1) interaction partners

1. Results suggest that PLAGL1 methylation is lower in very preterm infants compared to their full term counterparts, even when controlling for perinatal confounders

2. ZAC expression was studied in transgenic mice.

3. report here a novel PLAGL1 promoter (P5) derived from the insertion of a primate-specific, MIR3 SINE retrotransposon. P5 is highly utilized in lymphocytes, particularly in T cells, and like P2, directs biallelic transcription

4. Plagl1 is a transcription factor that coordinated the regulation of a subset of imprinted gene network genes and controlled extracellular matrix composition.

5. PLAGL1 methylation/expression may be altered after assisted reproductive technologies.

6. These results suggest that OCT attenuates SGC-7901 cell proliferation by enhancing P300-HAT activity through the interaction of ZAC and P300, causing a reduction in pS10-H3 and an increase in acK14-H3. These findings provide insight for future research on OCT and further demonstrate the potential of OCT to be used as a therapeutic agent for gastric cancer

7. High PLAGL1 mRNA and protein levels were associated with Clear Cell Renal Cell Carcinoma.

8. Results suggest that dysregulation of PLAGL1 expression may be involved in the progression of colorectal cancer (CRC) but the patient survival data do not confirm applicability of the PLAGL1 expression level as a prognostic factor in CRC.

9. Fetal growth can be influenced by altered expression of the PLAGL1 gene network in human placenta.

10. DNA deletion and promoter hyper-methylation both contribute to the down-regulation of PLAGL1 in gastric adenocarcinoma

11. There is positive correlations between the ZAC1 DMR methylation index (MI) and estimated fetal weight (EFW) at 32 weeks of gestation, weight at birth and weight at one year of age (respectively, r = 0.15, 0.09, 0.14; P values = 0.01, 0.15, 0.03).

12. research identified a specific CpG site where determination of the methylation status was associated with both metastasis-free and overall survival in undifferentiated sarcoma.

13. ZAC1 and SSTR2 are down-regulated in non-functioning pituitary adenomas but not in somatotropinomas.

14. Paternal methylation aberrations at imprinting control regions of DLK1-GTL2, MEST (PEG1), and ZAC (PLAGL1) and global methylation levels are not associated with idiopathic recurrent spontaneous miscarriages.

15. The imprinted PLAGL1 domain is flanked by CTCF-binding sites conserved between species in both expressing and non-expressing cells.

16. Based on these findings we conclude that the imprinted gene expression of KCNQ1OT1, CDKN1C, H19, and PLAGL1 are conserved between human and bovine

17. detected a synonymous variation in the protein-coding exon-2 of PLAGL1 in isolated VSD patients. It is possible that the etiology of isolated VSD might not be directly linked with this mutation

18. This work indicates that Zac1 functions are regulated, at least in part, via non-covalent interactions with SUMO-1 for the induction of p21, which is important for the modulation of apoptosis.

19. Zac1 is able to interact directly with the Sp1-responsive element in the p21(WAF1/Cip1) gene promoter.

20. The specific expression of ZAC in the human fetal beta-cells supports it as the gene involved in transient neonatal diabetes mellitus

Pig (Porcine) Pleiomorphic Adenoma Gene-Like 1 (PLAGL1) interaction partners

1. PLAGL1 is maternally imprinted in swine. Expression profiling using short-oligonucleotide microarrays of parthenotes and control fetal tissues supports imprinted isoform-specific expression.

2. The expression patterns of PLAGL1 and PEG10 genes in two breeds of swine are reported.

Mouse (Murine) Pleiomorphic Adenoma Gene-Like 1 (PLAGL1) interaction partners

1. PLAGL1 may regulate hypothalamic hypocretin transcription.

2. Zac1/GPR39 system promotes the formation of type II muscle fibers by phosphorylation of CaMK-II. Cells lacking Zac1/GPR39 system tend to remain stemness and form type I muscle fibers after induced differentiation.

3. Plagl1 is a transcription factor that coordinated the regulation of a subset of imprinted gene network genes and controlled extracellular matrix composition.

4. expression levels of Zac1 need to be kept under strict control to avoid premature cell cycle exit, disrupted neurogenesis and aberrant expression of non-neuronal genes including pluripotency associated factors.

5. Transcription factor MEF2 and Zac1 mediate MIF-induced GLUT4 expression through CD74-dependent AMPK activation in cardiomyocytes

6. we show that the maternally imprinted gene Zac1 is a critical regulator of neocortical development

7. Zac1 interacts with two cis-regulatory elements in the Tcf4 gene locus.

8. results indicate ZAC is a negative regulator of the acute stimulatory effects of glucose on beta-cells. It provides an explanation for both insulin deficiency in the neonate and the later relapse of diabetes in patients with transient neonatal diabetes mellitus cases

9. Hymai and Plagl1it RNAs both have potentially high affinity for Trithorax chromatin regulators.

10. identified the guanine nucleotide exchange factor Rasgrf1 as a direct Zac1/Plagl1 target gene in beta cells

11. Zac1 inhibits nuclear factor Kappa B activity by interacting with the C-terminus of the p65 subunit, which suppresses the phosphorylation of p65 at Ser468 and Ser536 residues

12. the different expression pattern of Zac1 in mice from human may explain the much milder phenotype in the mouse model of ZAC double dose

13. The Zac1 is a critical regulator of normal cerebellar development, adding a new transcriptional regulator to the growing list of factors involved in generating neuronal diversity in the developing cerebellum.

14. this study describes for the first time a transcriptional regulation of Zac1b, induced by synthetic dsRNA and RNA viruses

15. Plagl1/Zac1 gene is imprinted, with preferential expression from the paternal allele, and is one of a network of imprinted genes involved in the control of embryonic growth.

16. ZAC1 is a novel and previously unknown regulator of cardiomyocyte Glut4 expression and glucose uptake; MEF2 is a regulator of ZAC1 expression in response to induction of hypertrophy

17. Zac1 plays an essential role in the cardiac gene regulatory network. Data provide a potential link between Zac1 in cardiogenesis and congenital heart disease manifestations associated with genetic or epigenetic defects in an imprinted gene network.

18. Zac1 mRNA preferentially accumulates in close proximity to nucleoli within the cell nucleus.

19. Zac1 is a potential regulatory gene involved in chondrogenic differentiation.

20. Putative role in control of cell cycle and/or apoptosis. Strong induction observed in granular cells of dentate gyrus and in some glial cells of dentate gyrus and subventricular zone. Zac1 may be implicated in mechanisms of neural plasticity after injury.