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Human Polyclonal KL Primary Antibody pour ELISA, ICC - ABIN4329242
Manrique, Habibi, Aroor, Sowers, Jia, Hayden, Garro, Martinez-Lemus, Ramirez-Perez, Klein, Meininger, DeMarco: Dipeptidyl peptidase-4 inhibition with linagliptin prevents western diet-induced vascular abnormalities in female mice. dans Cardiovascular diabetology 2016
Human Polyclonal KL Primary Antibody pour WB - ABIN4890528
Chen, Gould, Garza, Gao, Hampton, Newton: Amplitude control of protein kinase C by RINCK, a novel E3 ubiquitin ligase. dans The Journal of biological chemistry 2007
Human Polyclonal KL Primary Antibody pour ELISA - ABIN450061
Chen, Podvin, Gillespie, Leeman, Abraham: Insulin stimulates the cleavage and release of the extracellular domain of Klotho by ADAM10 and ADAM17. dans Proceedings of the National Academy of Sciences of the United States of America 2007
Human Polyclonal KL Primary Antibody pour IHC (p), IHC - ABIN250843
Kurosu, Yamamoto, Clark, Pastor, Nandi, Gurnani, McGuinness, Chikuda, Yamaguchi, Kawaguchi, Shimomura, Takayama, Herz, Kahn, Rosenblatt, Kuro-o: Suppression of aging in mice by the hormone Klotho. dans Science (New York, N.Y.) 2005
Human Polyclonal KL Primary Antibody pour IF (p), IHC (p) - ABIN681778
Prudhomme, Glinka, Kurt, Liu, Wang: The anti-aging protein Klotho is induced by GABA therapy and exerts protective and stimulatory effects on pancreatic beta cells. dans Biochemical and biophysical research communications 2017
klotho protein could be considered as a protective factor against immunosenescent-like phenotype in monocytes an issue relevant to many immune disorders.
Results uncover a major mechanism of iPSC action, suggest a fundamental role of alphaKlotho in iPSC maintenance, and support the translational potential of airway delivery of cell-free iPSC secretome for protection against lung injury.
Serum klotho was an independent biomarker of left ventricular hypertrophy, but not arterial stiffness.
Gene expression array revealed that klotho and KL1 expression enhanced the unfolded protein response (UPR) and this was further established by increased levels of spliced XBP1, GRP78 and phosphorylated-eIF2alpha.
KLOTHO KL-VS polymorphism is associated with greater number of CD34+ and CD34+VEGFR2+ progenitor cells.
sKlotho is a biomarker of renal dysfunction and a potential treatment target for renoprotection in T2 diabetes mellitus.
Soluble klotho levels were inversely related to brain atrophy in alcoholic patients.
The tissue klotho protein expression was associated with a lower risk and progression of malignancies. Klotho may be a protective factor against malignancies risk/progression.
Serum Klotho may be a novel risk factor for atherosclerosis in maintenance hemodialysis patients
a single maximal aerobic exercise session of 20 min duration induced serum levels of klotho, particularly in women
Knockdown of klotho gene expression normalized IGF-1R and Wnt1 protein expressions and Akt phosphorylation in granulosa cells from patients with PCOS; it also blocked the effects of insulin on apoptosis and proliferation in granulosa cells.
Schizophrenia patients, KL-VS has a selective effect on memory, with heterozygotes in CD and CS clusters performing worse than non-carriers
The change in concentration of soluble alpha-klotho during the 1.5-years follow-up was an indicator of CKD progression. Renal damage associated with a reduction of alpha-klotho may involve the upregulation of plasma aldosterone.
Cord blood klotho levels were inversely correlated with leptin and insulin levels at birth
serum level of FGF-23 was not correlated with a change in bone mineral density of maintenance hemodialysis patients, whereas the serum Klotho protein level was associated with the degree of bone mineral density
solubility-Klotho level was closely correlated with kidney function
To evaluate the role of klotho in the pathogenesis of systemic sclerosis, its serum concentration was measured in patients compared to healthy controls, and its association with cutaneous and visceral involvement was assessed. Spearman's test showed no significant association between klotho serum levels and systemic sclerosis activity, concerning either clinical, laboratory or instrumental findings.
Klotho may play an inhibiting role in lipopolysaccharide-induced inflammation injury by inhibiting NF-kappaB and Wnt signaling pathways in HK-2 cells.
High klotho expression is associated with renal fibrosis and podocyte injuries.
Although our study revealed higher serum ET-1 and lower serum alpha-Klotho levels in systemic sclerosis patients compared to healthy controls, there were not any significant correlations between their serum levels with severity of organ involvement.
Depleting klotho selectively from the choroid plexus via targeted viral vector-induced knockout in Klotho mice increased the expression of multiple proinflammatory factors and triggered macrophage infiltration.
The present study analyzed the gene expression profile in salivary glands from accelerated aging klotho deficient mice.
The studies identify a role for alpha-Klotho in the regulation of muscle progenitor cell mitochondrial function and implicate alpha-Klotho declines as a driver of impaired muscle regeneration with age.
our study identified Klotho loss as a key event linking HDAC deregulation to the renal and bone injuries in CKD-MBD mice and demonstrated the therapeutic potentials of endogenous Klotho restoration by HDAC inhibition in treating CKD and the associated extrarenal complications.
Klotho has posed antioxidant and anti-apoptotic effects on oxidative injuries in TCMK-1 cells, which might be partially related to its inhibition of JNK/MAPK and p38/MAPK phosphorylation and subsequent elevation of antioxidant enzymes. Increasing Klotho expression has played a protective role against oxidative stress in tubular epithelial cells.
Klotho expression in the central nervous system is associated with total antioxidant capacity in mice with experimental autoimmune encephalomyelitis.
Using mouse strains with parathyroid-specific deletions of Klotho and CaSR and dual deletion of both genes, Klotho has a pivotal role in suppressing PTH in the absence of CaSR. Chronic hypocalcemia and ex vivo PTG culture demonstrated an independent role for Klotho in mediating PTH secretion.
DPP-4 inhibition with linagliptin slowed the progression of premature aging in klotho-/- mice. Provide a novel insight into the potential role of DPP-4 in the mechanism of premature aging.
Klotho protects tubular epithelial cells from renal ischemic-reperfusion injury and its anti-necroptotic role may be associated with oxidative stress inhibition.
studies uncover a novel hypomethylating character of Rhein in preventing Klotho loss and renal fibrosis, and demonstrate the efficacy of Klotho-targeted epigenetic intervention in potential treatment of renal fibrosis-associated kidney diseases.
the main physiological function of Klotho for mineral homeostasis in vivo is its role as co-receptor mediating Fgf23 action.
Findings establish a key role of osteocyte-expressed Klotho in regulating bone metabolism and indicate a new mechanism by which osteocytes control bone formation.
Selective HDAC3 inhibition effectively alleviated Klotho loss and kidney injury, whereas the protective effects were largely abolished when Klotho was knocked down by siRNA, suggesting that aberrant HDAC3 and Klotho loss are crucial components involved in the renal damage of mice with chronic kidney disease.
data showed that Klotho protects Tac-induced oxidative stress by negatively regulating the PI3K/AKT pathway and subsequently enhancing FoxO3a-mediated MnSOD expression.
The present study provides a novel approach for klotho gene therapy and demonstrates that direct up-regulation of klotho in the brain might improve aging-related memory impairments and decrease oxidative stress.
Klotho inhibits cigarette smoke-induced autophagy via down-regulation of IGF-1R, Akt, and ERK phosphorylation in alveolar macrophages.
In conclusion, the excessive 1,25(OH)2D3 formation in klotho-hypomorphic mice has a profound effect on murine behavior.
Klotho is a novel regulator of postnatal neurogenesis affecting neural stem cell proliferation and maturation sufficient to impact hippocampal-dependent spatial memory function.
Reduced Klotho expression aggravates tacrolimus-induced renal injury via the PI3K-Akt-FoxO pathway.
Two distinct isoforms of soluble Klotho appear to play counter-regulatory roles in cardiac fibrogenic responses.
Activated HAT activity of p300 modulates AV calcification through osteogenic transdifferentiation of VICs with Klotho modulation.
Klotho gene deficiency promotes high-fat diet-induced fibrosis in aortic valves, likely through the AMPKalpha-RUNX2 pathway.
significant expression of FGF23 and KL within the growth plate and adjacent tissues imply a potential local role of FGF23 in chondrocyte differentiation and tissue mineralization.
This gene encodes a type-I membrane protein that is related to beta-glucosidases. Reduced production of this protein has been observed in patients with chronic renal failure (CRF), and this may be one of the factors underlying the degenerative processes (e.g., arteriosclerosis, osteoporosis, and skin atrophy) seen in CRF. Also, mutations within this protein have been associated with ageing and bone loss.
secreted form of Klotho protein