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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 Kits (19) and GFER Proteins (18) and many more products for this protein.
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Human Polyclonal GFER Primary Antibody for ICC, IF - ABIN4313990
Ferecatu, Gonçalves, Golinelli-Cohen, Clémancey, Martelli, Riquier, Guittet, Latour, Puccio, Drapier, Lescop, Bouton: The diabetes drug target MitoNEET governs a novel trafficking pathway to rebuild an Fe-S cluster into cytosolic aconitase/iron regulatory protein 1. in The Journal of biological chemistry 2014
Data (including data from studies in knockout mice) suggest that KIBRA (show WWC1 Antibodies) plays important role in regulating HPO activity, YAP (show YAP1 Antibodies) signaling, and actin cytoskeletal dynamics in podocytes; expression of KIBRA (show WWC1 Antibodies) and YAP (show YAP1 Antibodies) plus phosphorylation of YAP (show YAP1 Antibodies) are up-regulated in glomeruli of patients with focal segmental glomerulosclerosis. (KIBRA (show WWC1 Antibodies) = kidney/brain protein-KIBRA (show WWC1 Antibodies); HPO = hepatopoietin protein; YAP (show YAP1 Antibodies) = Yes associated protein-1 (show YAP1 Antibodies))
Loss of DLG5 (show DLG5 Antibodies) expression promoted breast cancer progression by inactivating the Hippo signaling pathway and increasing nuclear YAP (show YAP1 Antibodies).
WWC2 functions as a tumor suppressor by negatively regulating the Hippo signaling pathway and may serve as a prognostic marker in hepatocellular carcinoma.
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.
IKBKE (show IKBKE Antibodies) 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.
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
ese findings collectively indicate that ALR negatively regulates the autophagy process through an association with the AMPK (show PRKAA1 Antibodies)/mTOR (show FRAP1 Antibodies) signaling pathway. Autophagy inhibit apoptosis and play a protective role under conditions of oxidative stress.
HPO interaction with MOB1 (show MOBKL3 Antibodies) is not essential for development and tissue growth control.
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 (show ABCB1 Antibodies) and ABCG2 signaling pathway.
ALR protects steatotic hepatocytes from ischemia reperfusion injury by attenuating oxidative stress and mitochondrial dysfunction.
To test whether differences in the ratio between CHCHD4 (show CHCHD4 Antibodies) and ALR might explain tissue-specific differences in the CHCHD4 (show CHCHD4 Antibodies) redox state, we determined the molar ratio of both proteins in different mouse tissues. Surprisingly, ALR is superstoichiometric over CHCHD4 (show CHCHD4 Antibodies) in most tissues.
The exogenous expression of hepatic stimulator substance (HSS (show PANK2 Antibodies) was renamed augmenter of liver regeneration ALR) protected the liver from steatosis in mice with nonalcoholic steatohepatitis.
this study shows that ALR can weaken ConA-induced hepatitis
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.
ALR can protect mice against acute liver injury by up-regulating the expression of regulatory T cells.
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
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.
ALR may serve as a potential diagnostic marker of hepatocellular stress and/or acute inflammatory conditions.
Growth factor erv1-like (Gfer) inhibits the COP9 (show COPS8 Antibodies) signalosome subunit jun activation-domain binding protein 1 (Jab1 (show COPS5 Antibodies))-mediated degradation of the cyclin-dependent kinase inhibitor p27(kip1 (show CDKN1B Antibodies)) to restrict proliferation of hematopoietic stem cells.
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 (show MFF Antibodies) Drp1 (show CRMP1 Antibodies).
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.
, 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)