Recombinant Human Hypoxia-inducible factor 3-alpha (HIF3A)

1. data suggest an important role of miR-210 in sustaining HIF-1alpha activity via the suppression of HIF-3alpha, regulating cell growth and chemotherapeutic drug resistance in cholangiocarcinoma. PMID: 29953500
2. AA can protect cardiomyocytes against hypoxia-induced apoptosis through regulating the miR-1290/HIF3A/HIF-1alpha axis, and miR-1290 may be a potential target in the prevention of myocardial ischemia-reperfusion injury PMID: 28686797
3. NAP peptide prevents outer blood retinal barrier breakdown by reducing HIF1alpha/HIF2alpha, VEGF/VEGFRs, and increasing HIF3alpha expression Moreover it is able to reduce the percentage of apoptotic cells by modulating the expression of two death related genes, BAX and Bcl2. PMID: 28436035
4. HIF3A methylation was found in the association between the HIF3A rs3826795 polymorphism and alanine aminotransferase among obese children. PMID: 28754107
5. TIMP2 suppression, in a hypoxic environment, was induced through a regulatory feedback circuit consisting of hypoxia-inducible factor (HIF) 1 alpha, microRNA-210 (miR-210), and HIF-3alpha. PMID: 27018975
6. Results were discordant with those expected if HIF3A methylation has a causal effect on body mass index (BMI) & provided more evidence for causality in the reverse direction (i.e., an effect of BMI on HIF3A methylation); results also show a long-lasting intergenerational influence of maternal BMI on offspring methylation at this locus, which may confound associations between own adiposity & HIF3A methylation. PMID: 26861784
7. DNA methylation in HIF3A shares moderate correlation between adipose tissue and blood, and both are associated with BMI. In contrast, methylation in FASN is poorly correlated across tissues, but the DNA methylation in adipose tissue but not blood is highly associated with BMI PMID: 26891033
8. Reduced lifetimes of the donor were partially restored by coexpression of HIF-1alpha or Bcl-xL, binding proteins of IPAS in the nucleus and mitochondria, respectively. PMID: 28003430
9. Results confirmed a positive association between BMI and HIF3A DNA promoter methylation in the blood. The tissue-specific results of HIF3A gene expression indicate that subcutaneous adipose tissue is the more functional tissue in which a low expression may adversely affect whole-body insulin sensitivity. PMID: 27594926
10. Parkin is downregulated under hypoxia and that it interferes with HIF expression based on cellular oxygen tension. PMID: 26742768
11. miR210 may be a negative regulator of the progression of osteoarthritis, which increases chondrocyte proliferation and prompts extracellular matrix deposition by directly targeting HIF3alpha. PMID: 26861791
12. This provides a compelling model for how hypoxia-induced miR-429 regulates the switch between HIF-1 adaptive responses to HIF-3 survival responses by rapidly decreasing HIF1A levels while simultaneously slowing the progression of HIF3A expression until the miR-429 levels drop below normoxic levels. PMID: 26954587
13. The association between increased DNA methylation at HIF3A and increased adiposity is present in neonates. PMID: 26011824
14. Unsaturated fatty acids are high-affinity ligands of the C-terminal domain from the HIF-3alpha. PMID: 26237540
15. HIF3A DNA Methylation Is Associated with Childhood Obesity and ALT PMID: 26717317
16. HIF3alpha has a transcriptional regulatory function, which negatively affects gene expression by competing with HIF1alpha and HIF2alpha in binding to transcriptional elements in target genes during hypoxia. (Review) PMID: 25936862
17. inverse association with hypertrophic markers in chondrogenic cells PMID: 26174816
18. A DNA methylation variant in HIF3A was associated with BMI changes through interactions with total or supplemental vitamin B2, vitamin B12, and folate. PMID: 26001398
19. Here we provide evidence for the miRNA mediated regulation of HIF3a by hypoxia responsive miRNAs in STS, which may help to tightly regulate and fine-tune the hypoxic response. PMID: 24927770
20. The Inhibitory Per/Arnt/Sim (PAS) domain protein (IPAS) is a splice variant of hypoxia-inducible factor (HIF)-3alpha, and possesses two entirely different functions. The results strongly suggest that IPAS is a nucleocytoplasmic shuttling protein. PMID: 24092767
21. These findings highlight the importance of the hypoxia-sensing pathway and HIFs in clinical hematology. PMID: 24371328
22. Were significantly upregulated in the HIF3alpha expressing lungs. PMID: 23451260
23. the transcription of HIF-3alpha4 was silenced by the promoter DNA methylation in meningiomas, and inducible HIF-3alpha4 impaired angiogenesis, proliferation, and metabolism/oxidation in hypervascular meningiomas PMID: 23485455
24. data indicate that the HIF-3alpha variants may have more versatile and specific roles in the regulation of the hypoxia response than previously anticipated PMID: 21479871
25. Cell-specific and hypoxia-dependent regulation of human HIF-3alpha. PMID: 21069422
26. It is a negative regulator of tumorigenesis. (review) PMID: 21404626
27. HIF3A is regulated by hypoxia in the developing human lung. PMID: 20551700
28. Hypoxia upregulated transcription from all three alternative HIF-3alpha promoters. siRNA experiments showed that this induction is mediated specifically by HIF-1 and not by HIF-2. PMID: 20416395
29. multiple splice variants of locus are targets of the von Hippel-Lindau E3 ubiquitin ligase complex PMID: 12538644
30. IPAS1 and IPAS2 inhibit angiogenesis by binding to and inhibiting HIF-1alpha and HIF-1beta. PMID: 16182248
31. findings suggest that HIF-3alpha, as a member of the HIF system, is complementary rather than redundant to HIF-1alpha induction in protection against hypoxic damage in alveolar epithelial cells. PMID: 16775626
32. The expression of HIF-3alpha4 suppresses the growth of tumor xenografts in SCID mice. PMID: 17998805
33. The findings shed light on a novel aspect of HIF-3alpha as a HIF-1 target gene and point to a possible role as a modulator of hypoxic gene induction. PMID: 19694616
34. The splice isoform HIF-3alpha4 inhibits transcription of VEGF and GLUT1 by binding to and inhibiting HIF-1alpha and HIF-1beta. PMID: 16126907

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HGNC: 15825

OMIM: 609976

KEGG: hsa:64344

STRING: 9606.ENSP00000366898

UniGene: Hs.420830