Ask about this productRelated genes to: ALPP antibody
- Gene:
- ALPG NIH gene
- Name:
- alkaline phosphatase, germ cell
- Previous symbol:
- ALPPL2
- Synonyms:
- GCAP
- Chromosome:
- 2q37.1
- Locus Type:
- gene with protein product
- Date approved:
- 1990-07-06
- Date modifiied:
- 2018-04-16
- Gene:
- ALPP NIH gene
- Name:
- alkaline phosphatase, placental
- Previous symbol:
- -
- Synonyms:
- PALP, PLAP
- Chromosome:
- 2q37.1
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2018-02-28
Related products to: ALPP antibody
Related articles to: ALPP antibody
- Human naive pluripotent stem cells established from the epiblasts of preimplantation blastocysts provide a useful model for mechanistic studies of pluripotency regulation and lineage differentiation. Important advances have been made to optimize culture conditions and define molecular criteria for naive pluripotency. However, the identity of naive-specific surface markers and the underlying molecular mechanism of naive pluripotency regulation remain poorly understood. Here, we identify alkaline phosphatase placental-like 2 (ALPPL2) as a prominent naive-specific surface marker by systematic proteomic and transcriptomic analyses. Furthermore, we demonstrate that ALPPL2 is essential for both the establishment and maintenance of naive pluripotency. Moreover, we show that ALPPL2 can interact with the RNA-binding protein IGF2BP1 to stabilize the mRNA levels of the naive pluripotency transcription factors TFCP2L1 and STAT3 to regulate naive pluripotency. Overall, our study identifies a functional surface marker for human naive pluripotency, providing a powerful tool for human-naive-pluripotency-related mechanistic studies. - Source: PubMed
Bi YanTu ZhifenZhang YanpingYang PengGuo MingyueZhu XuehaoZhao ChengchenZhou JianfengWang HongWang YixuanGao Shaorong - Alkaline phosphatase placental-like 2 (ALPPL2) is a member of the ALPP alkaline phosphatase family and is reported to be associated with the growth of some tumors. Gastric cancer is one of the most common cancers worldwide. We previously identified a distinct expression pattern of ALPPL2 between gastric cancer and adjacent normal tissues. In this study, we examined the expression of ALPPL2 in gastric adenocarcinoma and its ability to predict prognosis. We used bioinformatics analysis and immunohistochemistry to examine the expression pattern of ALPPL2 and analyzed the associations between ALPPL2 level and perioperative characteristics and the prognosis of gastric adenocarcinoma patients by Kaplan-Meier plotter analysis. Our results indicated that the expression of ALPPL2 was significantly increased in gastric adenocarcinoma (P < .01) and was an independent factor (P < .05) that could provide reliable prognostic information on gastric adenocarcinoma patients. High expression of ALPPL2 was associated with advanced TNM stage (P < .05) and high HER-2 expression (P < .01). Our study suggests that ALPPL2 has the potential to reveal prognostic information on gastric cancer. - Source: PubMed
Publication date: 2018/11/26
Liu ShuangMao QinshengXue WanjiangZhang XiaojingQi YueWang YingjingChen PeiZhou Qing - Nucleoside analogues are the most promising drugs for the treatment of pancreatic cancer to date. However, their use is often limited due to toxic side effects. Aptamer-mediated targeted delivery of these drugs to cancer cells could maximize their effectiveness and concomitantly minimize the toxic side effects by reducing uptake into normal cells. Previously, we identified a pancreatic cancer-specific, nuclease-resistant RNA aptamer, SQ2, which binds to alkaline phosphatase placental-like 2 (ALPPL2), a putative biomarker for pancreatic cancer. In this study, we demonstrate that the aptamer can be internalized into pancreatic cancer cells and can thus be used for the targeted delivery of therapeutics. Using the aptamer as a ligand, we established that glycophosphatidylinositol-anchored ALPPL2 is internalized by the cells through clathrin-independent and caveolae-dependent or dynamin-mediated cell-type-dependent pathways. Finally, we show that SQ2 can deliver nucleoside drug 5-fluoro-2'-deoxyuridine specifically to ALPPL2-expressing pancreatic cancer cells, inhibiting cell proliferation. - Source: PubMed
Publication date: 2015/04/28
Dua PoojaS SajeeshKim SoyounLee Dong-ki - Exon splicing enhancers (ESEs) overlap with amino acid coding sequences implying a dual evolutionary selective pressure. In this study, we map ESEs in the placental alkaline phosphatase gene (ALPP), absent in the corresponding exon of the ancestral tissue-non-specific alkaline phosphatase gene (ALPL). The ESEs are associated with amino acid differences between the transcripts in an area otherwise conserved. We switched out the ALPP ESEs sequences with the sequence from the related ALPL, introducing the associated amino acid changes. The resulting enzymes, produced by cDNA expression, showed different kinetic characteristics than ALPL and ALPP. In the organism, this enzyme will never be subjected to selection because gene splicing analysis shows exon skipping due to loss of the ESE. Our data prove that ESEs restrict the evolution of enzymatic activity. Thus, suboptimal proteins may exist in scenarios when coding nucleotide changes and consequent amino acid variation cannot be reconciled with the splicing function. - Source: PubMed
Publication date: 2014/04/01
Falanga AlessiaStojanović OzrenKiffer-Moreira TinaPinto SofiaMillán José LuisVlahoviček KristianBaralle Marco - Environmental factors such as tobacco smoking may have long-lasting effects on DNA methylation patterns, which might lead to changes in gene expression and in a broader context to the development or progression of various diseases. We conducted an epigenome-wide association study (EWAs) comparing current, former and never smokers from 1793 participants of the population-based KORA F4 panel, with replication in 479 participants from the KORA F3 panel, carried out by the 450K BeadChip with genomic DNA obtained from whole blood. We observed wide-spread differences in the degree of site-specific methylation (with p-values ranging from 9.31E-08 to 2.54E-182) as a function of tobacco smoking in each of the 22 autosomes, with the percent of variance explained by smoking ranging from 1.31 to 41.02. Depending on cessation time and pack-years, methylation levels in former smokers were found to be close to the ones seen in never smokers. In addition, methylation-specific protein binding patterns were observed for cg05575921 within AHRR, which had the highest level of detectable changes in DNA methylation associated with tobacco smoking (-24.40% methylation; p = 2.54E-182), suggesting a regulatory role for gene expression. The results of our study confirm the broad effect of tobacco smoking on the human organism, but also show that quitting tobacco smoking presumably allows regaining the DNA methylation state of never smokers. - Source: PubMed
Publication date: 2013/05/17
Zeilinger SonjaKühnel BrigitteKlopp NormanBaurecht HansjörgKleinschmidt AnjaGieger ChristianWeidinger StephanLattka EvaAdamski JerzyPeters AnnetteStrauch KonstantinWaldenberger MelanieIllig Thomas