Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Displays phosphatase activity for serine/threonine residues, and, dephosphorylates and activates MAP3K5 kinase. De plus, nous expédions PGAM5 Kits (9) et PGAM5 Protéines (7) et beaucoup plus de produits pour cette protéine.
Showing 10 out of 10 products:
The authors show that developmental mitochondrial unfolded protein response is necessary and sufficient to extend Drosophila lifespan, and identify Phosphoglycerate Mutase 5 (PGAM5) as a mediator of this response. Developmental mitochondrial stress leads to activation of FoxO (Montrer FOXO Anticorps), via Apoptosis Signal-regulating Kinase 1 (ASK1 (Montrer MAP3K5 Anticorps)) and Jun-N-terminal Kinase (JNK (Montrer MAPK8 Anticorps)).
the mushroom body may possess an apoptosis-dependent toxic function, the suppression of which by dPGAM5 appears to be crucial for heat shock resistance.
PGAM5 negatively regulates the PINK1 (Montrer PINK1 Anticorps) pathway related to maintenance of the mitochondria.
An intact complex of PGAM5-KEAP1 (Montrer KEAP1 Anticorps)-Nrf2 (Montrer GABPA Anticorps) preserves mitochondrial motility by suppressing dominant-negative KEAP1 (Montrer KEAP1 Anticorps) activity.
PGAM5 regulates histidine phosphorylation to control TCR activation of CD4 (Montrer CD4 Anticorps)-positive T cells.
Results indicate that a multiprotein complex including PGAM5, Bax (Montrer BAX Anticorps) and Drp1 (Montrer CRMP1 Anticorps) proteins specifically formed during intrinsic apoptosis induction.
Results identify a crucial role for RIPK3 (Montrer RIPK3 Anticorps)-PGAM5-Drp1 (Montrer CRMP1 Anticorps)/NFAT (Montrer NFATC1 Anticorps) signalling in NKT (Montrer SLC22A6 Anticorps) cell activation, and further suggest that RIPK3 (Montrer RIPK3 Anticorps)-PGAM5 signalling may mediate crosstalk between mitochondrial function and immune signalling.
The BCL2L1 (Montrer BCL2L1 Anticorps)-PGAM5-FUNDC1 (Montrer FUNDC1 Anticorps) axis is critical for receptor-mediated mitophagy.
Dephosphorylation of FUNDC1 (Montrer FUNDC1 Anticorps) by PGAM5 induces mitophagy.
PGAM5 is proteolytically processed, accumulates in the cytosol during apoptosis, and sensitizes cells to death.
Rhomboid protease PARL (Montrer PARL Anticorps) mediates the mitochondrial membrane potential loss-induced cleavage of PGAM5.
Experimental data indicate that the two splice variants of the mitochondrial protein (Montrer COX6B2 Anticorps) phosphatase PGAM5 are at the convergent point of multiple necrosis pathways.
The N terminus of the PGAM5 protein contains a conserved NXESGE motif that binds to the substrate binding pocket in the Kelch domain of Keap1 (Montrer KEAP1 Anticorps).
findings suggest that HO-1 (Montrer HMOX1 Anticorps) protects against I/R-induced hepatic injury via regulation of mitochondrial QC by PGAM5 signaling.
Taken together, our findings provide evidence that NBP can attenuate the progression of EAE by suppressing PGAM5-induced necroptosis and inflammation in microglia and represents a new therapeutic strategy for treating autoimmune diseases.
Results revealed that RIPK1 (Montrer RIPK1 Anticorps) and PGAM5 function independently to exert optimal control of Leishmania replication in the host.
Our data demonstrate for the first time that PGAM5 plays an indispensable role in the pathogenesis of ConA-induced liver injury.
we also found that Pgam5-deficient mice are resistant to high-fat-diet-induced obesity. Our study uncovered that PGAM5 is involved in the whole-body metabolism in response to stresses that impose metabolic challenges on mitochondria.
Our results revise the former proposal that PGAM5 acts downstream of RIP1 (Montrer RALBP1 Anticorps)/RIP3 (Montrer MPRIP Anticorps) to mediate necroptosis. Instead, PGAM5 protects cells from necroptosis by independently promoting mitophagy.
PGAM5 is a novel regulator of inflammasome and caspase 1 (Montrer CASP1 Anticorps) activity that functions independently of RIPK3 (Montrer RIPK3 Anticorps).
Results identify a crucial role for RIPK3 (Montrer RIPK3 Anticorps)-PGAM5-Drp1 (Montrer CRMP1 Anticorps)/NFAT (Montrer NFATC1 Anticorps) signalling in NKT (Montrer CTSL1 Anticorps) cell activation, and further suggest that RIPK3 (Montrer RIPK3 Anticorps)-PGAM5 signalling may mediate crosstalk between mitochondrial function and immune signalling.
Loss of PGAM5 disables PINK1 (Montrer PINK1 Anticorps)-mediated mitophagy in vitro and leads to dopaminergic neurodegeneration and mild dopamine loss in vivo causing a Parkinson's-like movement disorder.
Pgam5 is essential for head formation, and for establishing and maintaining the Wnt (Montrer WNT2 Anticorps)/beta-Catenin (Montrer CTNNB1 Anticorps) signaling gradient that patterns the anterior-posterior body axis. We show that Pgam5 interacts with Dishevelled2 and that Dishevelled2 is a substrate of Pgam5.
Displays phosphatase activity for serine/threonine residues, and, dephosphorylates and activates MAP3K5 kinase. Has apparently no phosphoglycerate mutase activity. May be regulator of mitochondrial dynamics. Substrate for a KEAP1-dependent ubiquitin ligase complex. Contributes to the repression of NFE2L2- dependent gene expression (By similarity).
, phosphoglycerate mutase 5
, Bcl-XL-binding protein v68
, serine/threonine-protein phosphatase PGAM5, mitochondrial