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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 (17) and many more products for this protein.
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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.
Our results show that MARK4 (show MARK4 Antibodies) acts as a negative regulator of the Hippo kinase cassette to promote YAP (show YAP1 Antibodies)/TAZ (show TAZ Antibodies) activity and that loss of MARK4 (show MARK4 Antibodies) restrains the tumorigenic properties of breast cancer cells.
ALR, dependent on its localization, changes the acute-phase response (APR (show LRP1 Antibodies)) at least in part, by modifying STAT3 (show STAT3 Antibodies) activation; dual signaling of ALR suggests that ALR is pivotal for the regulation of APR (show LRP1 Antibodies), a crucial event in liver injury and regeneration
the mechanistic regulation and linkage of the ROR1 (show ROR1 Antibodies)-HER3 (show ERBB3 Antibodies) and Hippo-YAP (show YAP1 Antibodies) pathway in a cancer-specific context
S100A7 (show S100A7 Antibodies) induction by the Hippo-YAP (show YAP1 Antibodies) pathway in cervical and glossopharyngeal squamous cell carcinoma has been described.
FAT1 (show FAT1 Antibodies) protein acts upstream of Hippo signalling through TAZ (show TAZ Antibodies) protein to regulate neuronal differentiation.
ALR protects cells from apoptosis partly through increased autophagy in HepG2 cells.
Knockdown of GFER exerts anti-inflammatory actions via suppression of the mitogen-activated protein kinase (show MAPK1 Antibodies) signaling pathway
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).
Growth factor erv1-like modulates Drp1 (show CRMP1 Antibodies) to preserve mitochondrial dynamics and function in mouse embryonic stem cells
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.
, Kabuki make-up syndrome
, Kabuki mental retardation syndrome
, histone-lysine N-methyltransferase 2D
, histone-lysine N-methyltransferase MLL2
, lysine N-methyltransferase 2D
, myeloid/lymphoid or mixed-lineage leukemia 2
, trinucleotide repeat containing 21
, 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)