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Human HIF1A Protein expressed in Wheat germ - ABIN1306618
Vadivel, Alphonse, Etches, van Haaften, Collins, OReilly, Eaton, Thébaud: Hypoxia-inducible factors promote alveolar development and regeneration. in American journal of respiratory cell and molecular biology 2014
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A global reduction in Hif1a gene dosage increases predisposition of the offspring exposed to maternal diabetes to cardiac dysfunction. Hif1a is a critical factor in the fetal programming of adult cardiovascular disease.
HIF-1alpha regulation through hypoxic alveolar epithelial cells is critical to the initiation of acute inflammation after lung contusion.
HIF-1alpha stabilization could have a temporal neuroprotective effect on photoreceptor cell survival, glial activation, and antioxidant response at early stages of retinitis pigmentosa.
The data suggest that TFAF6 inhibition reduces choroidal neovascularization formation via down-regulating expression of HIF-1a and VEGF and activation of macrophages and microglia.
results provide the first evidence for a role of HIF-1alpha in the pathogenesis of lupus
MiR-497 approximately 195 cluster regulates angiogenesis during coupling with osteogenesis by maintaining endothelial Notch1 and HIF1A activity.
Biochemical studies identify a Bmp-mTORC1-Hif1a signaling cascade resulting in upregulation of Glut1 in chondrocytes that is essential for murine skeletal development.
Study shows that GLP-1 receptor signalling promotes beta-cell glucose metabolism via mTOR-dependent HIF-1alpha activation. findings suggest that chronic GLP-1 actions on insulin secretion include elevated beta-cell glucose metabolism. Moreover, our data reveal novel aspects of GLP-1 stimulated insulin secretion involving de novo gene expression.
HIF-1alpha activation in myeloid cells critically regulates Inflammatory bowel disease progression.
HOXA9 inhibits HIF1A-mediated glycolysis through interacting with CRIP2 to repress cutaneous squamous cell carcinoma development.
Overexpression of HIF1A leads to radioresistance of cervical cancer.
Studies demonstrate a role for HIF-1alpha in regulation of TSP2 expression via primarily a transcriptional mechanism.
HIF1alpha role in the cardiac hypertrophy, apoptosis, and fibrosis.HIF1alpha is partially inhibited in the cardiac fibrosis by p53.
T3 thyroid hormone increased HIF-1alpha protein levels as well as steroid secretion in Leydig cells
Myeloid-specific deletion of Hif1a had no impact on the number of myeloid cells migrating into the eye.
HS-induced PPARalpha-mediated downregulation of PHD1 is a novel pathway for PHD/HIF-1alpha transcriptional regulation.
HIF1alpha promoted macrophage glycolysis metabolism, which induced M1 polarization in mice.
DAPK deficiency leads to excess HIF-1a accumulation, enhanced IL-17 expression and exacerbated experimental autoimmune encephalomyelitis.
activation of HIF signaling in osteoprogenitor cells increases blood levels of the chemokine C-X-C motif ligand 12, which leads to a systemic increase of breast cancer cell proliferation and dissemination through direct activation of the CXCR4 receptor
HIF regulation of HOIL-1L targets the phosphorylated PKC-zeta for degradation and serves as an hypoxia-adaptive mechanism to stabilize the Na,K-ATPase, avoiding significant lung injury.
In a hypoxic model of cell line ARPE-19, an increased expression level of ANG and induction of EMT accompanied with stabilization and nucleus translocation of HIF-1alpha. Blockage of HIF-1alpha signaling resulted in inhibition of high expression of ANG and EMT features.
HIF1A single nucleotide polymorphism rs11549465 T showed the reverse association with primary varicose veins risk
Sirtuin type 1 (SIRT1) and hypoxia-inducible factor 1, alpha subunit (HIF1alpha) associated-metabolism is closely linked to immune-associated diseases, including itumors and inflammation [Review].
MALAT1, acting through HIF-1alpha stabilization, is a mediator that enhances glycolysis induced by arsenite. These results provide a link between the induction of lncRNAs and the glycolysis in cells exposed to arsenite, and thus establish a previously unknown mechanism for arsenite-induced hepatotoxicity.
Studied role of MicroRNA 429 on hypoxia tolerance thru regulation of expression of hypoxia inducible factor 1 subunit alpha in human amniotic mesenchymal stem cells.
High glucose affected the expression of angiogenic factors in choriocarcinoma cells via the PKCbeta and HIF-1alpha pathways, suggesting their involvement in preeclampsia pathogenesis.
This study identified collagen XV as a new low O2 tension sensitive gene, and provided a novel mechanistic evidence that directly HIF-1alpha (hypoxia-inducible factor-1 alpha) mediates collagen XV expression in response to hypoxia, since it was found specifically in vivo recruited at collagen XV promoter, in hypoxia-preconditioned mesenchymal stromal cells.
High PGK1 expression was associated with poor prognosis in breast cancer, because PGK1 and HIF-1alpha formed a positive feed-forward loop and thus stimulated breast cancer progression and metastases.
hypoxia promotes the viability of cardiac stem cells in serum-free medium by HIF-1alpha/NDUFA4L2 signaling pathway.
MIR31HG is a HIF-1alpha co-activator that regulates the HIF-1 transcriptional network, crucial for cancer development.
High HIF1A expression is associated with peritoneal dissemination in gastric cancer.
ANGPTL4 was immunohistochemically detectable in 76 out of 109 osteosarcoma cases. ANGPTL4 was induced by hypoxia in 6 osteosarcoma cell lines, under the control of the HIF-1alpha transcription factor.
By modulating alpha ketoglutarate (alpha-KG) and succinate levels Collagen prolyl 4-hydroxylase alpha 1 subunit (P4HA1) protein expression reduces proline hydroxylation on hypoxia-inducible factor (HIF) 1alpha, enhancing its stability in cancer cells. P4HA1 promotes chemoresistance by modulating HIF-1-dependent cancer cell stemness.
we found that there was a significant association of HIF-1alpha polymorphism in exon 12 among DFU patients when compared to control groups. The circulatory HIF-1alpha protein expression study indicated a decreased expression in DFU levels when compared to T2DM and control.
This study demonstrated that Hypoxia-Inducible Factor 1alpha and AT-Rich Interactive Domain-Containing Protein 1A Expression in Pituitary Adenomas.
hypoxic mRNA stabilization is independent of HIF transcriptional activity but requires mitochondrial reactive oxygen species.
These data suggest that HIF-1alpha-dependent regulation of glycolysis is necessary for maximum glucose metabolism in brown adipocytes
These findings demonstrated a valuable antitumor synergism in combining CRISPR/Cas9mediated HIF1alpha knockout with Transarterial embolization (TAE)in mice and highlighted the possibility that HIF1a may be an effective therapeutic knockout target in combination with TAE for hepatocellular carcinoma treatment
Since the FIH-1 dependent hydroxylation of NAA10 occurs oxygen-dependently, NAA10 acetylates HIF-1alpha under normoxia but does not under hypoxia.
HIF1A is upregulated in breast and bladder tumors with high NRF2 activity. NRF2 targets a functional antioxidant response element at the HIF1A locus, which reveals a direct regulatory connection between two important oxygen responsive transcription factors.
results of the present study suggest that increases in hypoxia inducible factor 1 subunit alpha( HIF-1alpha) are responsible for initial response to hypoxia that results in a transient cell cycle arrest in trophectoderm cells
The results showed that 60-min ischemia of the porcine uterus conducted at the mid-secretory estrous phase caused decreased HIF-1alpha and increased SOD-2 gene expression.
a high expression of hypoxia induced factor-1a (HIF-1a) and heat shock protein 70 (HSP70) was noted
Induction of ischemic osteonecrosis results in IL-6 production in the articular cartilage through an HIF-1-dependent pathway.
Upregulation of VEGF during hypoxia in chondrocyte is mediated partially through HIF-1alpha.
HIF-1alpha activates Sox9 expression and enhances Sox9-mediated transcriptional activity.
Intramyocardial delivery of mesenchymal stem cells seems to trigger the release of angiogenic HIF-1alpha more effectively than does intracoronary delivery.
immunostaining for HIF-1alpha and HIF-2alpha was observed during endochondral ossification, whereas only HIF-2alpha was present at sites of intramembranous ossification
Downregulation of miR-199a derepresses hypoxia-inducible factor-1alpha and Sirtuin 1 and recapitulates hypoxia preconditioning in cardiac myocytes.
Viable chondrocytes in the superficial layer of the epiphyseal cartilage showed HIF-1alpha activation and VEGF upregulation with subsequent revascularization occurring in the cartilage.
inverse expression and localization pattern of HIF1A and vasohibins during different stages of ovarian function in cow
changes in hypoxia-associated gene expression during the lactation cycle
Hypoxia increased the amounts of HIF1A protein, VEGF mRNA and VEGF protein in cultured bovine luteal cells.
hypoxia-induced changes in vascular cell growth are altered by hyperglycemia via inhibition of HIF-1alpha expression and activity
VEGF has an effect on the expression of its own transcription factor, HIF-1, and on VEGF itself
Identify sphingosine-1-phosphate as a novel and potent nonhypoxic activator of HIF-1.
Suggest supplemental oxygen inhibits HIF-1alpha/VEGF signaling to reduce smooth muscle proliferation in rabbit arteriovenous fistula model.
HIF-1alpha-induced HSP70 overexpression increased the expression levels of ECM genes and cell viability, and protected chondrocytes from apoptosis. HIF-1alpha may regulate anabolic effects of chondrocytes under hypoxic conditions by regulating HSP70 expression
Transcatheter arterial embolization of liver tumors increases the expression of HIF-1alpha at protein level in the residual viable tumor.
Upregulation of HIF-1 protects cardiac myocyte function after ischemia/reperfusion by maintaining calcium release.
HIF-1alpha expression in early atherosclerosis can promote the formation of neovascularization.
Xells respond to hypoxia through a transcription factor, hypoxia-inducible factor 1
Upregulation of HIF-1 could protect isolated cardiac myocytes against nitrate tolerance through a cyclic GMP protein kinase-independent mechanism and through a kinase-dependent mechanism in myocardial stunning.
rhEPO can down-regulate HIF-1alpha expression in the retina of rabbits with acute high intraocular pressure.
Increased HIF-1 alpha protects the functional effects of cyclic GMP thorough maintenance of cyclic GMP protein kinase activity after ischemic-reperfusion
Our results suggest that these detoxification pathways are mediated by the hypoxia inducible factor HIF-1. Finally, we show that sulfide resistance varies among wild C. elegans and other nematode species, suggesting that tolerance to sulfide was naturally selected in certain habitats.
blocking HIF-1 activity may promote survival in cells with compromised mitochondrial function.
HIF-1-mediated activation of 5-HT signalling promotes axon regeneration by activating both the RhoA and cAMP pathways.
this study reports that neuronal stabilization of HIF-1 mediates these effects in Caenorhabditis elegans through a cell nonautonomous signal to the intestine, which results in activation of the xenobiotic detoxification enzyme flavin-containing monooxygenase-2 (FMO-2).
AMPK and HIF-1 may control immunity and longevity tightly by acting as feedback regulators of ROS
Growth in hypoxia increases longevity in wild-type worms but not in animals lacking HIF-1 or DAF-16. Conversely, hypoxia shortens life span in combination with overexpression of the antioxidant stress response protein SKN-1.
HIF can function either as a gene-specific inducer or repressor of host defense, providing a molecular mechanism by which HIF can have apparently opposing roles in defense and inflammation.
Increased levels of hydrogen peroxide induce a HIF-1-dependent modification of lipid metabolism in AMPK compromised C. elegans dauer larvae.
These data show that HIF-1 regulates intestinal iron homeostasis during iron deficiency by activating and inhibiting genes involved in iron uptake and storage.
Data indicate that genes sqrd-1, ethe-1, cysl-1, cysl-2 and HIF-1 are involved in survival to hydrogen sulfide and hydrogen cyanide.
Data show that stabilization of HIF-1 increases life span robustly under all conditions tested; however, deletion of hif-1 increases life span in a temperature-dependent manner.
Data show that that reactive oxygen species (ROS) are increased in respiration mutants and that mild increases in ROS can stimulate HIF-1 to activate gene expression and promote longevity.
These data support a model in which SWAN-1, MBK-1 and EGL-9 regulate HIF-1 transcriptional activity and modulate C. elegans resistance to P. aeruginosa PAO1 fast killing.
transgerminal neuroectodermal conversion of hMSCs into NSC-like cells is accompanied by extensive changes of their global gene expression profile, which might be controlled in part by transcription factor networks related to HIF-1 and miR-124a
The antiapoptotic property of HIF-1 is mediated by means of transcriptional upregulation of the tyrosinase family member TYR-2 in the ASJ sensory neurons
Data show that EGL-9 inhibits HIF-1 transcriptional activity via a pathway that has little or no requirement for hydroxylase activity or for the EGL-9 MYND domain.
HIF-1 upregulation is both an evolutionarily conserved and a necessary component of heat acclimation.
In Caenorhabditis elegans the product of the hif-1 gene plays a crucial role in heat adaptation.
studies identified hypoxia-regulated gene expression changes requiring hypoxia-inducible transcription factor (HIF-1) function in response to low oxygen levels
The Caenorhabditis elegans rhy-1 gene inhibits hif-1 activity in a negative feedback loop that does not include vhl-1.
This gene encodes the alpha subunit of transcription factor hypoxia-inducible factor-1 (HIF-1), which is a heterodimer composed of an alpha and a beta subunit. HIF-1 functions as a master regulator of cellular and systemic homeostatic response to hypoxia by activating transcription of many genes, including those involved in energy metabolism, angiogenesis, apoptosis, and other genes whose protein products increase oxygen delivery or facilitate metabolic adaptation to hypoxia. HIF-1 thus plays an essential role in embryonic vascularization, tumor angiogenesis and pathophysiology of ischemic disease. Alternatively spliced transcript variants encoding different isoforms have been identified for this gene.
, HIF1 alpha
, Hypoxia-inducible factor 1 alpha
, hypoxia-inducible factor 1-alpha
, ARNT-interacting protein
, ARNT interacting protein
, PAS domain-containing protein 8
, basic-helix-loop-helix-PAS protein MOP1
, class E basic helix-loop-helix protein 78
, hypoxia-inducible factor 1 alpha isoform I.3
, hypoxia-inducible factor 1, alpha subunit (basic helix-loop-helix transcription factor)
, hypoxia-inducible factor1alpha
, member of PAS protein 1
, member of PAS superfamily 1
, hypoxia-inducible factor 1 alpha
, hypoxia inducible factor 1 alpha subunit
, hypoxia inducible factor 1, alpha subunit