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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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T3 thyroid hormone (zeige PTH Proteine) 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 (zeige PPARA Proteine)-mediated downregulation of PHD1 (zeige EGLN2 Proteine) is a novel pathway for PHD (zeige PDC Proteine)/HIF-1alpha transcriptional regulation.
HIF1alpha promoted macrophage glycolysis metabolism, which induced M1 polarization in mice.
DAPK (zeige DAPK1 Proteine) deficiency leads to excess HIF-1a accumulation, enhanced IL-17 (zeige IL17A Proteine) 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 (zeige CXCL12 Proteine), which leads to a systemic increase of breast cancer cell proliferation and dissemination through direct activation of the CXCR4 (zeige CXCR4 Proteine) receptor
HIF regulation of HOIL-1L (zeige RBCK1 Proteine) targets the phosphorylated PKC-zeta (zeige PRKCZ Proteine) for degradation and serves as an hypoxia-adaptive mechanism to stabilize the Na,K-ATPase (zeige ATP1A1 Proteine), avoiding significant lung injury.
our study suggests that HIF1A is a common critical downstream mediator for HLH. We propose that HIF1A activation as the consequence of systemic inflammation, cytokine storm, or ligation of TLR may contribute to HLH development.
Decreased HIF-1alpha may contribute to impaired megakaryopoiesis in immune thrombocytopenia.
The results collectively suggest that in the pressure overload heart failure model, HSF1 (zeige HSF1 Proteine) promoted formation of macrophages by inducing upregulation of HIF-1 expression, through which heart failure was ameliorated.
Findings revealed an HIF-1alpha/IL-1beta (zeige IL1B Proteine) signaling loop between cancer cells and tumor-associated macrophages in a hypoxic microenvironment, resulting in cancer cell epithelial-mesenchymal transition and metastasis; more importantly, our results suggest a potential role of an anti-inflammatory strategy in hepatocellular carcinoma treatment
Overexpression of HIF-1alpha and P4HB (zeige P4HB Proteine) is associated with poor prognosis in patients with gastric cancer.
hypoxic stress in the hepatocellular carcinoma (HCC)cells promoted YAP binding to HIF-1a in the nucleus and sustained HIF-1a protein stability to bind to PKM2 gene and directly activates PKM2 transcription to accelerate glycolysis
Overexpression of VHL was more successful at inhibiting fibrosis compared with silencing HIF-1a plus HIF-2a. Normoxia-active HIF-1a or HIF-2a prevented the inhibitory effect of VHL on liver fibrosis, indicating that attenuating fibrosis via VHL is HIF-1a- and HIF-2a-dependent to some extent.
Results find that knockdown of HIF-1alpha reduced hypoxia-induced SENP1 (zeige SENP1 Proteine) expression, suggesting that induction of SENP1 (zeige SENP1 Proteine) expression is mediated by hypoxia-inducible factor HIF-1alpha.
ADM (zeige ADM Proteine) was an upstream molecule of HIF-1alpha/VEGF (zeige VEGFA Proteine) and it promoted angiogenesis through upregulating HIF-1alpha/VEGF (zeige VEGFA Proteine) in epithelial ovarian cancer.
HIF-1alpha expression correlates with the expression level of IL- 8 (zeige IL8 Proteine), as evidenced by the down regulation of IL-8 (zeige IL8 Proteine) in response to silencing of HIF-1alpha in HCC (zeige FAM126A Proteine) cell lines under hypoxic conditions.
MOLP8/R cells display a very high overexpression of LCP1 (zeige LCP1 Proteine) gene (l-Plastin (zeige LCP1 Proteine)) controlled by HIF1&alpha.
the role of FTH1 (zeige FTH1 Proteine) in the FIH (zeige CASR Proteine) control of HIF-1 activity, is reported.
The findings of the current study demonstrate presence of the IDH1 (zeige IDH1 Proteine) R132H mutation in primary human glioblastoma cell lines with upregulated HIF-1alpha expression, downregulating c-MYC (zeige MYC Proteine) activity and resulting in a consequential decrease in miR (zeige MLXIP Proteine)-20a, which is responsible for cell proliferation and resistance to standard temozolomide treatment.
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 (zeige SOD2 Proteine) gene expression.
a high expression of hypoxia induced factor-1a (HIF-1a) and heat shock protein 70 (HSP70 (zeige HSP70 Proteine)) was noted
Induction of ischemic osteonecrosis results in IL-6 (zeige IL6 Proteine) production in the articular cartilage through an HIF-1-dependent pathway.
Upregulation of VEGF (zeige VEGFA Proteine) during hypoxia in chondrocyte is mediated partially through HIF-1alpha.
HIF-1alpha activates Sox9 (zeige SOX9 Proteine) expression and enhances Sox9 (zeige SOX9 Proteine)-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 (zeige EPAS1 Proteine) was observed during endochondral ossification, whereas only HIF-2alpha (zeige EPAS1 Proteine) was present at sites of intramembranous ossification
Downregulation of miR (zeige MYLIP Proteine)-199a derepresses hypoxia-inducible factor-1alpha and Sirtuin 1 (zeige SIRT1 Proteine) and recapitulates hypoxia preconditioning in cardiac myocytes.
Viable chondrocytes in the superficial layer of the epiphyseal cartilage showed HIF-1alpha activation and VEGF (zeige VEGFA Proteine) 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
Hypoxia increased the amounts of HIF1A protein, VEGF (zeige VEGFA Proteine) mRNA and VEGF (zeige VEGFA Proteine) 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 (zeige VEGFA Proteine) has an effect on the expression of its own transcription factor, HIF-1, and on VEGF (zeige VEGFA Proteine) itself
Identify sphingosine-1-phosphate as a novel and potent nonhypoxic activator of HIF-1.
Suggest supplemental oxygen inhibits HIF-1alpha/VEGF (zeige VEGFA Proteine) signaling to reduce smooth muscle proliferation in rabbit arteriovenous fistula model.
HIF-1alpha-induced HSP70 (zeige HSP70 Proteine) overexpression increased the expression levels of ECM (zeige MMRN1 Proteine) genes and cell viability, and protected chondrocytes from apoptosis. HIF-1alpha may regulate anabolic effects of chondrocytes under hypoxic conditions by regulating HSP70 (zeige HSP70 Proteine) 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 (zeige SQRDL Proteine) resistance varies among wild C. elegans and other nematode species, suggesting that tolerance to sulfide (zeige SQRDL Proteine) 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 (zeige DDC Proteine) signalling promotes axon regeneration by activating both the RhoA (zeige RHOA Proteine) 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 (zeige FMO2 Proteine)).
AMPK (zeige PRKAA1 Proteine) and HIF-1 may control immunity and longevity tightly by acting as feedback regulators of ROS (zeige ROS1 Proteine)
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.
Increased levels of hydrogen peroxide induce a HIF-1-dependent modification of lipid metabolism in AMPK (zeige PRKAA1 Proteine) 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 (zeige ETHE1 Proteine), cysl-1, cysl-2 and HIF-1 are involved in survival to hydrogen sulfide (zeige SQRDL Proteine) 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.
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