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Autophagy is the process by which endogenous proteins and damaged organelles are destroyed intracellularly. De plus, nous expédions ATG4B Protéines (13) et beaucoup plus de produits pour cette protéine.
Showing 10 out of 179 products:
Human Polyclonal ATG4B Primary Antibody pour IHC (p), WB - ABIN388494
Baehrecke: Autophagy: dual roles in life and death? dans Nature reviews. Molecular cell biology 2005
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Human Polyclonal ATG4B Primary Antibody pour IF, IHC (p) - ABIN1882065
Pontén, Westermark: Properties of human malignant glioma cells in vitro. dans Medical biology 1978
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Human Polyclonal ATG4B Primary Antibody pour EIA, IHC (p) - ABIN1449637
Lum, DeBerardinis, Thompson: Autophagy in metazoans: cell survival in the land of plenty. dans Nature reviews. Molecular cell biology 2005
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Human Polyclonal ATG4B Primary Antibody pour EIA, IHC (p) - ABIN1449638
Greenberg: Degrade or die: a dual function for autophagy in the plant immune response. dans Developmental cell 2005
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Human Polyclonal ATG4B Primary Antibody pour IHC (p), WB - ABIN388497
Tanida, Sou, Ezaki, Minematsu-Ikeguchi, Ueno, Kominami: HsAtg4B/HsApg4B/autophagin-1 cleaves the carboxyl termini of three human Atg8 homologues and delipidates microtubule-associated protein light chain 3- and GABAA receptor-associated protein-phospholipid conjugates. dans The Journal of biological chemistry 2004
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Human Monoclonal ATG4B Primary Antibody pour WB - ABIN659121
Satoo, Noda, Kumeta, Fujioka, Mizushima, Ohsumi, Inagaki: The structure of Atg4B-LC3 complex reveals the mechanism of LC3 processing and delipidation during autophagy. dans The EMBO journal 2009
Cow (Bovine) Polyclonal ATG4B Primary Antibody pour IHC, WB - ABIN2787433
Olsen, Blagoev, Gnad, Macek, Kumar, Mortensen, Mann: Global, in vivo, and site-specific phosphorylation dynamics in signaling networks. dans Cell 2006
Cow (Bovine) Polyclonal ATG4B Primary Antibody pour WB - ABIN2775794
Kumanomidou, Mizushima, Komatsu, Suzuki, Tanida, Sou, Ueno, Kominami, Tanaka, Yamane: The crystal structure of human Atg4b, a processing and de-conjugating enzyme for autophagosome-forming modifiers. dans Journal of molecular biology 2005
These results support the conclusion that CML24 affects autophagy progression through interactions with ATG4.
AtATG4a is catalytically more active and has broad AtATG8 substrate specificity compared with AtATG4b. [ATG4b]
The structure and regulatory machinery of Atg4b [review]
MIRlet-7i is able to regulate autophagic activity via regulating Atg4B expression, which might contribute to the pathogenesis of pre-eclampsia.
The results have interesting implications that SLC27A4 (Montrer SLC27A4 Anticorps)/ATG4B complex might be conducive to the occurrence of autophagy in human cancer cells, which is meaningful investigations toward the aim of developing autophagy-targeting drugs and have significant values in clinical application.
Results demonstrated that upregulation of miR (Montrer MLXIP Anticorps)-34a by transfection or demethylation resulted in the enhanced apoptosis and drug sensitivity in prostate cancer cells. ATG4B, directly regulated by miR (Montrer MLXIP Anticorps)-34a through AMPK (Montrer PRKAA1 Anticorps)/mTOR (Montrer FRAP1 Anticorps), was involved in this process.
Purified ATG4B protein interact with LC3B (Montrer MAP1LC3B Anticorps) in vitro.
ATG4B independently plays a role as a positive regulator on tumor proliferation and a negative regulator on autophagy in colorectal cancer cells.
This study identifies ATG4B as a potential biomarker for predicting therapeutic response in treatment-naive chronic myeloid leukemia (Montrer BCL11A Anticorps) stem/progenitor cells and uncovers ATG4B as a possible drug target in these cells.
The actions of ATG4 family members (particularly ATG4B) are required for the control of autophagosome fusion with late, degradative compartments in differentiating human erythroblasts.
Atg4B possessed the broadest spectrum against all substrates, followed by Atg4A (Montrer ATG4A Anticorps) for ATG8 (Montrer GABARAPL2 Anticorps) substrates
HsAtg4B negatively regulates the localization of LC3 (Montrer MAP1LC3A Anticorps) to a membrane compartment by delipidation
miR (Montrer MLXIP Anticorps)-34a might regulate the autophagic activity and can cause injury in ischemia reperfusion injured renal tubular epithelial cells (RTEC) via targeting Atg4B. Atg4B knockdown inhibited autophagy in RTECs.
the ATG4B protease and autophagy play a crucial role protecting epithelial cells against bleomycin-induced stress and apoptosis
REDD1 (Montrer DDIT4 Anticorps)/TXNIP (Montrer TXNIP Anticorps) complex expression is sufficient to induce reactive oxygen species, suppress ATG4B activity and activate autophagy.
these findings demonstrate a role for Ser (Montrer SIGLEC1 Anticorps)-383 and Ser (Montrer SIGLEC1 Anticorps)-392 phosphorylation of ATG4B in control of autophagy.
mTOR (Montrer FRAP1 Anticorps) inhibition alleviates Huntington's disease progression by inducing Atg4b-dependent autophagic flux.
An autophagy-related gene, Atg4b, is identified as a de novo target gene of C/EBP BETA (Montrer CEBPB Anticorps) and is shown to play an important role in 3T3-L1 adipocyte differentiation.
the RNF5-mediated control of membranalATG4B reveals a novel layer in the regulation of LC3 (Montrer MAP1LC3A Anticorps) processing and autophagy.
The Atg4b participates in polarized secretion of lysosomal contents into the extracellular space by directing lysosomes to fuse with the plasma membrane.
Genetic inactivation of mouse Atg4b resulted in amorphous globular bodies in the neuropil of the deep cerebellar nuclei and adjacent vestibular nuclei and a mild but measurable impairment of motor performance on the Rotarod.
The Apg4B/autophagin-1 protease thus serves as a processing/deconjugating enzyme for these four highly divergent mammalian Apg8 homologues, GATE-16 (Montrer GABARAPL2 Anticorps), MAP1 (Montrer MOAP1 Anticorps)-LC3 (Montrer MAP1LC3A Anticorps), GABARAP (Montrer GABARAP Anticorps), and Apg8L (Montrer GABARAPL1 Anticorps).
Autophagy is the process by which endogenous proteins and damaged organelles are destroyed intracellularly. Autophagy is postulated to be essential for cell homeostasis and cell remodeling during differentiation, metamorphosis, non-apoptotic cell death, and aging. Reduced levels of autophagy have been described in some malignant tumors, and a role for autophagy in controlling the unregulated cell growth linked to cancer has been proposed. This gene encodes a member of the autophagin protein family. The encoded protein is also designated as a member of the C-54 family of cysteine proteases. Alternate transcriptional splice variants, encoding different isoforms, have been characterized.
ATG4 autophagy related 4 homolog B
, cysteine protease ATG4B
, autophagy 4b variant 1Cysteine protease ATG4B
, autophagy 4b variant 3
, cysteine protease ATG4b
, APG4 autophagy 4 homolog B
, autophagy-related protein 4 homolog B
, autophagy-related cysteine endopeptidase 2B
, AUT-like 1 cysteine endopeptidase
, autophagy-related cysteine endopeptidase 1
, APG4 (ATG4) autophagy-related homolog B
, AUT-like 1, cysteine endopeptidase
, autophagin 1
, autophagy-related 4B
, cysteine protease involved in autophagy APG4-B
, autophagy related 4 homolog B
, autophagy related 4-like protein B