anti-Pleckstrin Homology-Like Domain, Family A, Member 2 (PHLDA2) Antikörper

Human Pleckstrin Homology-Like Domain, Family A, Member 2 (PHLDA2) Interaktionspartner

1. Authors demonstrated that TSSC3 was an independent prognostic marker for overall survival in osteosarcoma, and positive ATG5 expression associated with positive TSSC3 expression suggested a favorable prognosis for patients. Then, we showed that TSSC3 overexpression enhanced autophagy via inactivating the Src-mediated PI3K/Akt/mTOR pathway in osteosarcoma.

2. RanBP9/TSSC3 complex cooperatively suppress metastasis via downregulation of Src-dependent Akt pathway to expedite mitochondrial-associated anoikis.

3. PHLDA2 plays an important role in the occurrence and development of pregnancy complications by promoting trophoblast apoptosis and suppressing cell invasion.

4. TSSC3 was a prognostic marker in osteosarcoma.

5. TSSC3 downregulation promotes the Epithelial to mesenchymal transition (EMT) of osteosarcoma cells by regulating EMT markers via a signal transduction pathway that involves Snail, Wnt-beta-catenin/TCF, and GSK-3beta

6. Placental PHLDA2 expression was significantly 2.3 fold higher in reduced fetal movements pregnancies resulting in delivery of a growth restricted compared with a normal birth weight infant.

7. PHLDA2 may promote the occurrence/development of preeclampsia by inhibiting proliferation/migration/invasion of trophoblasts.

8. The gene expression pattern of CDKN1C, H19, IGF2, KCNQ1 and PHLDA2 genes was evaluated using RT-PCR.

9. elevated expression in placenta of growth restricted pregnancies [review]

10. results suggest upregulated pleckstrin homology-like domain family A member 2 (PHLDA2) in placenta of monozygotic twins may be associated with the pathogenesis of singleton intrauterine growth restriction

11. TSSC3 overexpression suppressed osteosarcoma cell growth and increased apoptosis through caspase-3 upregulation, suggesting that TSSC3 may play a pro-apoptosis role to maintain the normal balance of growth

12. TSSC3 inhibits osteosarcoma tumorigenicity through reducing stemness and promoting apoptosis of tumor inducing cells

13. A luciferase reporter assay was used to identify in the PHLDA2 promoter a 15 bp repeat sequence variant that significantly reduces PHLDA2-promoter efficiency. Maternal inheritance of the variant resulted in a significant increase in birth weight.

14. The results suggest that placental PHLDA2 may provide a biomarker for suboptimal skeletal growth in pregnancies uncomplicated by overt fetal growth restriction.

15. TSSC3 has a potent tumor suppressor role in osteosarcoma, probably by inhibition of growth and induction of apoptosis via the mitochondrial apoptosis pathway.

16. PHLDA2 is a target gene of the BACH1 transcription factor according to ChIP-seq analysis in HEK 293 cells.

17. Expression levels of PHLDA2 gene were upregulated in the first trimester pregnancy

18. PHLDA2 gene is imprinted, with preferential expression from the maternal allele in placenta and liver.

19. Transcripts of TSSC3 could not be detected in human oocytes and preimplantation embryos.

20. Exposure of trophoblasts to hypoxia in vitro markedly reduced the expression of PHLDA2.

Mouse (Murine) Pleckstrin Homology-Like Domain, Family A, Member 2 (PHLDA2) Interaktionspartner

1. Phlda2 manipulates the placenta's demands for maternal resources, a process that must be tightly regulated by epigenetic marks to ensure optimal foetal growth.

2. data support a direct role for elevated Phlda2 in limiting fetal growth but also suggest that growth restriction only manifests when there is limited placental reserve

3. TSSC3 plays an important role in the differentiation from trophoblast stem cell to trophoblast progenitors and/or labyrinth trophoblasts through the TSSC3/PI3K/AKT/MASH2 signaling pathway.

4. Phlda2 gene is imprinted, with preferential expression from the maternal allele in placenta. It acts as a rheostat for placental growth, with overgrowth after gene deletion and growth retardation after loss of imprinting.

5. A critical role for the imprinted Phlda2 gene in regulating glycogen storage in the eutherian placenta is identified.

6. deletion causes placental overgrowth

7. Embryonic expression of Ipl in mice

8. Ipl and Tih1 are bona fide PH domain proteins, with broad specificity and moderate affinity for PIPs.

Pig (Porcine) Pleckstrin Homology-Like Domain, Family A, Member 2 (PHLDA2) Interaktionspartner

1. In the present study, a 259 base pair-specific sequence for IPL gene of the domestic pig was obtained and a novel SNP, a T/C transition, was identified in IPL exon 1. Variable imprinting status of this gene was observed in different developmental stages.

2. Quantitative allelic sequencing supports maternal expression of PHLDA2 in fetal liver and placental tissues using an interbreed swine model.

Cow (Bovine) Pleckstrin Homology-Like Domain, Family A, Member 2 (PHLDA2) Interaktionspartner

1. genes critical for placental development were altered in nuclear transfer placentas, including an imprinted gene. Allele-specific changes in the permissive histone mark in the PHLDA2 promoter indicate misregulation of imprinting in clones.

2. imprinting status of four cattle genes (Tssc4,Nap1l4, Phlda2 and Osbpl5) in seven types of tissues, were assessed in cattle.

3. proper expression levels of the imprinted genes CDKN1C and PHLDA2 are critical for embryo development

4. Pleckstrin homology-like domain family A member 2 (PHLDA2) gene is expressed across a range of cattle fetal tissues and stages. It provides the first evidence that PHLDA2 is a monoallelically expressed imprinted gene in cattle fetal tissues and placenta.