Growth Factor, Augmenter of Liver Regeneration Proteine (GFER)

The hepatotrophic factor designated augmenter of liver regeneration (ALR) is thought to be one of the factors responsible for the extraordinary regenerative capacity of mammalian liver. Zusätzlich bieten wir Ihnen GFER Antikörper (87) und GFER Kits (19) und viele weitere Produktgruppen zu diesem Protein an.

alle Proteine anzeigen Gen GeneID UniProt
GFER 2671 P55789
Ratte GFER GFER 27100 Q63042
GFER 11692 P56213
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Top GFER Proteine auf antikoerper-online.de

Showing 10 out of 15 products:

Katalog Nr. Origin Quelle Konjugat Bilder Menge Anbieter Lieferzeit Preis Details
Insektenzellen Human His tag „Crystallography Grade“ protein due to multi-step, protein-specific purification process 1 mg Anmelden zum Anzeigen 50 Days
$6,749.58
Details
Insektenzellen Maus His tag „Crystallography Grade“ protein due to multi-step, protein-specific purification process 1 mg Anmelden zum Anzeigen 50 Days
$6,749.58
Details
HEK-293 Cells Human Unkonjugiert 10 μg Anmelden zum Anzeigen 2 bis 3 Tage
$385.00
Details
Human Cells Human His tag 100 μg Anmelden zum Anzeigen 14 bis 16 Tage
$505.35
Details
Escherichia coli (E. coli) Human His tag   50 μg Anmelden zum Anzeigen 4 Days
$313.50
Details
Wheat germ Human GST tag 10 μg Anmelden zum Anzeigen 11 bis 12 Tage
$340.00
Details
Escherichia coli (E. coli) Human His tag 50 μg Anmelden zum Anzeigen 15 bis 19 Tage
$400.00
Details
HEK-293 Cells Human Myc-DYKDDDDK Tag Validation with Western Blot 20 μg Anmelden zum Anzeigen 11 Days
$888.80
Details
Escherichia coli (E. coli) Human His tag   10 μg Anmelden zum Anzeigen 15 bis 16 Tage
$212.50
Details
HEK-293 Cells Human Unkonjugiert   20 μg Anmelden zum Anzeigen 2 bis 3 Tage
$515.63
Details

GFER Proteine nach Spezies und Herkunft

Origin Exprimiert in Konjugat
Human , , , ,
, ,
Mouse (Murine) ,
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Weitere Proteine zu Growth Factor, Augmenter of Liver Regeneration (GFER) Interaktionspartnern

Human Growth Factor, Augmenter of Liver Regeneration (GFER) Interaktionspartner

  1. Data (including data from studies in knockout mice) suggest that KIBRA plays important role in regulating HPO activity, YAP signaling, and actin cytoskeletal dynamics in podocytes; expression of KIBRA and YAP plus phosphorylation of YAP are up-regulated in glomeruli of patients with focal segmental glomerulosclerosis. (KIBRA = kidney/brain protein-KIBRA; HPO = hepatopoietin protein; YAP = Yes associated protein-1)

  2. Loss of DLG5 expression promoted breast cancer progression by inactivating the Hippo signaling pathway and increasing nuclear YAP.

  3. WWC2 functions as a tumor suppressor by negatively regulating the Hippo signaling pathway and may serve as a prognostic marker in hepatocellular carcinoma.

  4. the results of this study demonstrated that targeted inhibition of the ALR expression in Jurkat cells triggered cell growth inhibition and sensitized cells to VCR via promoting apoptosis and regulating the cell cycle.

  5. IKBKE plays a pivotal role in regulating cell proliferation, invasion and epithelial-mesenchymal transition of malignant glioma cells in vitro and in vivo by impacting on the Hippo pathway.

  6. we found 2 additional patients carrying compound heterozygous variants in GFER. Reverse phenotyping confirmed the phenotypical similarities between the 4 patients. Together with the first literature reports, the review of these 8 cases from 4 unrelated families enables us to better describe this apparently homogeneous disorder, with the clinical and biological stigmata of mitochondrial disease

  7. ese findings collectively indicate that ALR negatively regulates the autophagy process through an association with the AMPK/mTOR signaling pathway. Autophagy inhibit apoptosis and play a protective role under conditions of oxidative stress.

  8. HPO interaction with MOB1 is not essential for development and tissue growth control.

  9. Overexpression of augmenter of liver regeneration (ALR) in liver cancer was studied and found to improve sensitivity to antitumor drugs by increasing the retention of intracellular drugs, at least partly through the modulation of the ABCB1 and ABCG2 signaling pathway.

  10. role in regulating the mitochondrial fission machinery

  11. It evidence demonstrating Hippo-independent regulation of TEADs and the potential impacts these studies may have on new cancer therapeutics.

  12. ALR protects steatotic hepatocytes from ischemia reperfusion injury by attenuating oxidative stress and mitochondrial dysfunction.

  13. Our results show that MARK4 acts as a negative regulator of the Hippo kinase cassette to promote YAP/TAZ activity and that loss of MARK4 restrains the tumorigenic properties of breast cancer cells.

  14. ALR, dependent on its localization, changes the acute-phase response (APR) at least in part, by modifying STAT3 activation; dual signaling of ALR suggests that ALR is pivotal for the regulation of APR, a crucial event in liver injury and regeneration

  15. the mechanistic regulation and linkage of the ROR1-HER3 and Hippo-YAP pathway in a cancer-specific context

  16. S100A7 induction by the Hippo-YAP pathway in cervical and glossopharyngeal squamous cell carcinoma has been described.

  17. FAT1 protein acts upstream of Hippo signalling through TAZ protein to regulate neuronal differentiation.

  18. ALR protects cells from apoptosis partly through increased autophagy in HepG2 cells.

  19. Knockdown of GFER exerts anti-inflammatory actions via suppression of the mitogen-activated protein kinase signaling pathway

  20. ALR plays a protective role against hydrogen peroxide-induced oxidative stress in renal proximal tubule cells.

Mouse (Murine) Growth Factor, Augmenter of Liver Regeneration (GFER) Interaktionspartner

  1. Study in mouse model of liver cirrhosis demonstrate that the lack of ALR aggravates liver fibrosis, probably by regulating mitochondrial Ca2+ homeostasis and mitochondrial dynamics in hepatic stellate cells.

  2. To test whether differences in the ratio between CHCHD4 and ALR might explain tissue-specific differences in the CHCHD4 redox state, we determined the molar ratio of both proteins in different mouse tissues. Surprisingly, ALR is superstoichiometric over CHCHD4 in most tissues.

  3. role in regulating the mitochondrial fission machinery

  4. The exogenous expression of hepatic stimulator substance (HSS was renamed augmenter of liver regeneration ALR) protected the liver from steatosis in mice with nonalcoholic steatohepatitis.

  5. this study shows that ALR can weaken ConA-induced hepatitis

  6. ALR is apparently required to ensure appropriate liver regeneration following PH in mice, and deletion of the ALR gene may delay liver regeneration in part due to impaired mitochondrial biogenesis.

  7. ALR can protect mice against acute liver injury by up-regulating the expression of regulatory T cells.

  8. From weeks 2-4 after birth, levels of steatosis and apoptosis decreased in ALR-L-KO mice, and numbers of ALR-expressing cells increased, along with ATP level

  9. As a mechanism, we suggest a direct protective effect of ALR on apoptotic and necrotic death of hepatocytes and an attenuation of inflammatory cell influx into the postischemic tissue.

  10. ALR may serve as a potential diagnostic marker of hepatocellular stress and/or acute inflammatory conditions.

  11. Growth factor erv1-like (Gfer) inhibits the COP9 signalosome subunit jun activation-domain binding protein 1 (Jab1)-mediated degradation of the cyclin-dependent kinase inhibitor p27(kip1) to restrict proliferation of hematopoietic stem cells.

  12. Gfer plays an essential pro-survival role in the maintenance of murine embryonic stem cell pluripotency by preserving the structural and functional integrity of their mitochondria, through modulation of the key mitochondrial fission factor Drp1.

  13. Growth factor erv1-like modulates Drp1 to preserve mitochondrial dynamics and function in mouse embryonic stem cells

  14. studies demonstrated a specific accumulation of full-length mouse Alrp during the early stages of spermatogenesis; the highest levels of Alrp were found in spermatogonia and primary spermatocytes

  15. review of the molecular biology of ALR [review]

GFER Protein Überblick

Protein Überblick

The hepatotrophic factor designated augmenter of liver regeneration (ALR) is thought to be one of the factors responsible for the extraordinary regenerative capacity of mammalian liver. It has also been called hepatic regenerative stimulation substance (HSS). The gene resides on chromosome 16 in the interval containing the locus for polycystic kidney disease (PKD1). The putative gene product is 42% similar to the scERV1 protein of yeast. The yeast scERV1 gene had been found to be essential for oxidative phosphorylation, the maintenance of mitochondrial genomes, and the cell division cycle. The human gene is both the structural and functional homolog of the yeast scERV1 gene.

Genbezeichner und Symbole assoziert mit GFER

  • growth factor, augmenter of liver regeneration (GFER)
  • growth factor, augmenter of liver regeneration (Gfer)
  • growth factor, augmenter of liver regeneration L homeolog (gfer.L)
  • Alr Protein
  • ERV1 Protein
  • HERV1 Protein
  • HPO Protein
  • HPO1 Protein
  • HPO2 Protein
  • HSS Protein

Bezeichner auf Proteinebene für GFER

ERV1 homolog , FAD-linked sulfhydryl oxidase ALR , erv1-like growth factor , hepatic regenerative stimulation substance , hepatopoietin protein , augmenter of liver regeneration , growth factor, erv1 homolog , growth factor, erv1-like (augmenter of liver regeneration) , growth factor, augmenter of liver regeneration , growth factor, augmenter of liver regeneration (ERV1 homolog, S. cerevisiae)

GENE ID SPEZIES
2671 Homo sapiens
27100 Rattus norvegicus
479885 Canis lupus familiaris
618423 Bos taurus
694203 Macaca mulatta
733269 Xenopus laevis
750034 Pan troglodytes
11692 Mus musculus
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