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anti-Human Endonuclease G Anticorps:
anti-Mouse (Murine) Endonuclease G Anticorps:
anti-Rat (Rattus) Endonuclease G Anticorps:
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Human Polyclonal Endonuclease G Primary Antibody pour IHC (p), IHC - ABIN265775
Jacquemin, Margiotta, Kasahara, Bassoy, Walch, Thiery, Lieberman, Martinvalet: Granzyme B-induced mitochondrial ROS are required for apoptosis. dans Cell death and differentiation 2015
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Cow (Bovine) Polyclonal Endonuclease G Primary Antibody pour WB - ABIN2784751
Varecha, Amrichová, Zimmermann, Ulman, Lukásová, Kozubek: Bioinformatic and image analyses of the cellular localization of the apoptotic proteins endonuclease G, AIF, and AMID during apoptosis in human cells. dans Apoptosis : an international journal on programmed cell death 2007
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Human Polyclonal Endonuclease G Primary Antibody pour IHC (p), WB - ABIN2473433
de-Mattos-Pimenta, Tiedemann: Hemispheric asymmetries in the recognition of animal photographs in different views. dans Brazilian journal of medical and biological research = Revista brasileira de pesquisas médicas e biológicas / Sociedade Brasileira de Biofísica ... [et al.] 1992
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Dog (Canine) Polyclonal Endonuclease G Primary Antibody pour ELISA, IHC - ABIN4308033
Chiu, Cheng, Lin, Chang, Liou, Lai: Bupivacaine induces apoptosis through caspase-dependent and -independent pathways in canine mammary tumor cells. dans Research in veterinary science 2015
These data indicated the participation of EndoG in alternative mRNA splicing of the telomerase catalytic subunit (Montrer TERT Anticorps) hTERT, regulation of telomerase activity and determination of cell fate.
Galectin-3 (Montrer LGALS3 Anticorps)-induced cell death in HIV-1-infected macrophages is most likely related to the translocation of Endo G from the cytoplasm to the nucleus.
ndoG digests long non-coding RNA and produces 47-mer (Montrer MERTK Anticorps) RNA oligonucleotide complementary to hTERT pre-mRNA exon 8 and intron 8 junction place. Interaction of 47-mer (Montrer MERTK Anticorps) RNA oligonucleotide and hTERT pre-mRNA causes alternative splicing.
Overexpression of EndoG in CD4 (Montrer CD4 Anticorps)+ T cells downregulated the expression of the active full-length hTERT variant and upregulated the inactive alternatively spliced variant.
Overexpression of EndoG in capital ES, Cyrillicsmall a, Cyrilliccapital ES, Cyrillicsmall o, Cyrillic-2 cells downregulated the expression of active full-length hTERT variant and upregulated non-active spliced variant.
EndoG is not a mediator of exogenous DNA clearance, but in non-physiological circumstances, it may nonspecifically cleave intracellular DNA regardless of its origin.
These findings suggest that non-viral DNA vectors are also substrates for EndoG in its role in homologous recombination
our study established a link between Endo G and mitochondrial function during cardiac hypertrophy
Results show that BNIP3 (Montrer BNIP3 Anticorps) interacts with the voltage-dependent anion channel (VDAC) to directly induce mitochondrial release and nuclear translocation of EndoG.
Endonuclease G (EndoG), an apoptotic nuclease (Montrer DCLRE1C Anticorps), as an essential factor for MLLbcr-specific DNA recombination after induction of replication stress.
These results support the involvement of redox signaling in the control of cardiomyocyte growth by ENDOG and suggest a pathway relating mtDNA content to the regulation of cell growth probably involving humanin, which prevents reactive oxygen radicals accumulation and hypertrophy induced by Endog deficiency.
Deficiency of AKT2 (Montrer AKT2 Anticorps) in myocardium results in diminished MEF2A (Montrer MEF2A Anticorps) abundance, which induced decreased size of cardiomyocytes. We additionally confirmed that EndoG, which is also regulated by AKT2 (Montrer AKT2 Anticorps), is a suppressor of MEF2A (Montrer MEF2A Anticorps) in myocardium.
increased browning of white adipose tissue elicited by the lack of EndoG was associated with a better glucose tolerance and reduced fat mass
This study demonistated that Endonuclease G knockout mice reveals a new putative molecular player in the regulation of anxiety.
These findings determine a role for EndoG in the generation of Switch region double-strand DNA breaks and class switch DNA recombination.
EndoG is essential during early embryogenesis and plays a critical role in normal apoptosis and nuclear DNA fragmentation
endonuclease G is essential for embryonic survival, but not through a mitochondrial or apoptosis function
These data suggest that the early nuclear translocation of endoG occurs and could induce DNA fragmentation in the ischemic brain after cerebral ischemia.
EndoG null mice are viable and develop to adulthood with no obvious abnormalities, suggesing that EndoG is not essential for early embryogenesis and apoptosis.
Overexpression of DNase I (Montrer DNASE1 Anticorps) in cultured mouse tubular epithelial cells also induced EndoG. Both DNase I (Montrer DNASE1 Anticorps) and EndoG mediate cisplatin injury to tubular epithelial cells.
Results describe the mechanism of catalysis and substrate binding by the apoptotic mitochondrial nuclease (Montrer DCLRE1C Anticorps) EndoG, which belongs to the large family of DNA/RNA non-specific betabetaalpha-Me-finger nucleases.
The protein encoded by this gene is a nuclear encoded endonuclease that is localized in the mitochondrion. The encoded protein is widely distributed among animals and cleaves DNA at GC tracts. This protein is capable of generating the RNA primers required by DNA polymerase gamma to initiate replication of mitochondrial DNA.
, TBC1 domain family, member 13
, endonuclease G, mitochondrial
, endonuclease G, mitochondrial-like
, endo G
, mitochondrial endonuclease G