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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.
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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 (Montrer IKBKE Anticorps) 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 (Montrer PRKAA1 Anticorps)/mTOR (Montrer FRAP1 Anticorps) signaling pathway. Autophagy inhibit apoptosis and play a protective role under conditions of oxidative stress.
HPO interaction with MOB1 (Montrer MOBKL3 Anticorps) 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 (Montrer ABCB1 Anticorps) and ABCG2 signaling pathway.
ALR protects steatotic hepatocytes from ischemia reperfusion injury by attenuating oxidative stress and mitochondrial dysfunction.
Our results show that MARK4 (Montrer MARK4 Anticorps) acts as a negative regulator of the Hippo kinase cassette to promote YAP (Montrer YAP1 Anticorps)/TAZ (Montrer TAZ Anticorps) activity and that loss of MARK4 (Montrer MARK4 Anticorps) restrains the tumorigenic properties of breast cancer cells.
ALR, dependent on its localization, changes the acute-phase response (APR (Montrer LRP1 Anticorps)) at least in part, by modifying STAT3 (Montrer STAT3 Anticorps) activation; dual signaling of ALR suggests that ALR is pivotal for the regulation of APR (Montrer LRP1 Anticorps), a crucial event in liver injury and regeneration
the mechanistic regulation and linkage of the ROR1 (Montrer ROR1 Anticorps)-HER3 (Montrer ERBB3 Anticorps) and Hippo-YAP (Montrer YAP1 Anticorps) pathway in a cancer-specific context
The exogenous expression of hepatic stimulator substance (HSS (Montrer PANK2 Anticorps) 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 (Montrer COPS8 Anticorps) signalosome subunit jun activation-domain binding protein 1 (Jab1 (Montrer COPS5 Anticorps))-mediated degradation of the cyclin-dependent kinase inhibitor p27(kip1 (Montrer CDKN1B Anticorps)) 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 (Montrer MFF Anticorps) Drp1 (Montrer CRMP1 Anticorps).
Growth factor erv1-like modulates Drp1 (Montrer CRMP1 Anticorps) 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.
, 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)