Growth Factor, Augmenter of Liver Regeneration (GFER) ELISA Kits

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. Additionally we are shipping GFER Antibodies (86) and GFER Proteins (15) and many more products for this protein.

list all ELISA KIts Gene Name GeneID UniProt
GFER 2671 P55789
GFER 27100 Q63042
GFER 11692 P56213
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Top GFER ELISA Kits at antibodies-online.com

Showing 10 out of 19 products:

Catalog No. Reactivity Sensitivity Range Images Quantity Supplier Delivery Price Details
Human 4.68 pg/mL 18.75-1200 pg/mL Typical standard curve 96 Tests Log in to see 15 to 18 Days
$910.56
Details
Mouse 29 pg/mL 78.12 pg/mL - 5000 pg/mL 96 Tests Log in to see 13 to 16 Days
$757.89
Details
Rabbit 1.0 pg/mL 250-5000 pg/mL   96 Tests Log in to see 15 to 18 Days
$707.14
Details
Guinea Pig 1.0 pg/mL 250-5000 pg/mL   96 Tests Log in to see 15 to 18 Days
$707.14
Details
Rat 0.1 ng/mL 0.5-10 ng/mL   96 Tests Log in to see 15 to 18 Days
$707.14
Details
Monkey 0.1 ng/mL 0.5-10 ng/mL   96 Tests Log in to see 15 to 18 Days
$707.14
Details
Pig
  96 Tests Log in to see 15 to 18 Days
$707.14
Details
Dog 1.0 pg/mL 250-5000 pg/mL   96 Tests Log in to see 15 to 18 Days
$707.14
Details
Chicken
  96 Tests Log in to see 15 to 18 Days
$707.14
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Sheep
  96 Tests Log in to see 15 to 18 Days
$707.14
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More ELISA Kits for GFER Interaction Partners

Human Growth Factor, Augmenter of Liver Regeneration (GFER) interaction partners

  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) interaction partners

  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 Antigen Profile

Antigen Summary

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.

Gene names and symbols associated with GFER

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

Protein level used designations for 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 SPECIES
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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