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Autophagy is the process by which endogenous proteins and damaged organelles are destroyed intracellularly. 再加上，我们可以发ATG4B 蛋白 (13)和数多这个蛋白质的别的产品。
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Human Polyclonal ATG4B Primary Antibody for IF, IHC (p) - ABIN1882065
Pontén, Westermark: Properties of human malignant glioma cells in vitro. in Medical biology 1978
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Human Polyclonal ATG4B Primary Antibody for WB - ABIN1881082
Kabeya, Mizushima, Yamamoto, Oshitani-Okamoto, Ohsumi, Yoshimori: LC3, GABARAP and GATE16 localize to autophagosomal membrane depending on form-II formation. in Journal of cell science 2004
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Human Polyclonal ATG4B Primary Antibody for IHC (p), WB - ABIN388494
Baehrecke: Autophagy: dual roles in life and death? in Nature reviews. Molecular cell biology 2005
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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]
Knockdown of ATG4B had only a minor effect on AMPK (显示 PRKAA1 抗体) activation and G1 phase arrest in liver kinase B1 (显示 STK11 抗体)-deficient or AMPK (显示 PRKAA1 抗体)-inhibited cancer cells.
Our work describes an MST4 (显示 MST4 抗体)-ATG4B signaling axis that influences glioblastoma autophagy and malignancy
Data show that ULK1 (显示 ULK1 抗体), a protein kinase (显示 CDK7 抗体) activated at the autophagosome formation site, phosphorylates human ATG4B on serine 316.
Reporter assay showed that HSF1 (显示 HSF1 抗体) increased the transcriptional activity of ATG4B gene promoter, and chromatin immunoprecipitation assay verified that HSF1 (显示 HSF1 抗体) bound to the site (-1429 to -1417) in ATG4B gene promoter region.
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 (显示 SLC27A4 抗体)/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 (显示 MLXIP 抗体)-34a by transfection or demethylation resulted in the enhanced apoptosis and drug sensitivity in prostate cancer cells. ATG4B, directly regulated by miR (显示 MLXIP 抗体)-34a through AMPK (显示 PRKAA1 抗体)/mTOR (显示 FRAP1 抗体), was involved in this process.
Purified ATG4B protein interact with LC3B (显示 MAP1LC3B 抗体) in vitro.
ATG4B independently plays a role as a positive regulator on tumor proliferation and a negative regulator on autophagy in colorectal cancer cells.
miR (显示 MLXIP 抗体)-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 (显示 DDIT4 抗体)/TXNIP (显示 TXNIP 抗体) complex expression is sufficient to induce reactive oxygen species, suppress ATG4B activity and activate autophagy.
these findings demonstrate a role for Ser (显示 SIGLEC1 抗体)-383 and Ser (显示 SIGLEC1 抗体)-392 phosphorylation of ATG4B in control of autophagy.
mTOR (显示 FRAP1 抗体) 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 (显示 CEBPB 抗体) 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 (显示 MAP1LC3A 抗体) 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 (显示 GABARAPL2 抗体), MAP1 (显示 MOAP1 抗体)-LC3 (显示 MAP1LC3A 抗体), GABARAP (显示 GABARAP 抗体), and Apg8L (显示 GABARAPL1 抗体).
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