Cysteine protease ATG4B Antibodies

Cysteine protease ATG4B (ATG4B)

Cysteine protease required for the cytoplasm to vacuole transport (Cvt) and autophagy. Cleaves the C-terminal amino acid of ATG8 family proteins MAP1LC3, GABARAPL1, GABARAPL2 and GABARAP, to show a C-terminal glycine.

Exposure of the glycine at the C- terminus is essential for ATG8 proteins conjugation into phosphatidylethanolamine (PE) and insertion to membranes, which is essential for autophagy. Has also an activity of delipidating receptor to the PE-conjugated forms.

Gene Information

Human
Gene Name:	ATG4B
Uniprot:	Q9Y4P1
Entrez:	23192

Family

Belongs to:
peptidase C54 family

Alternative Names

APG4 autophagy 4 homolog B (S. cerevisiae); APG4 autophagy 4 homolog B; Apg4B; ATG4 autophagy related 4 homolog B (S. cerevisiae); ATG4B; AUTL1; AUTL1MGC1353; AUT-like 1 cysteine endopeptidase; autophagin-1; Autophagy-related cysteine endopeptidase 1; Autophagy-related protein 4 homolog B; cysteine protease ATG4B; DKFZp586D1822; EC 3.4.22; EC 3.4.22.-; hAPG4B; KIAA0943

Molecular Weight

Mass (kDA):
44.294 kDA

Genomic Context

Human
Location:	2q37.3
Sequence:	2; NC_000002.12 (241637659..241673857)

Tissue Specificity

Mainly expressed in the skeletal muscle, followed by brain, heart, liver and pancreas.

Subcellular Localizations

Cytoplasm.

Diseases

• Nerve Degeneration
• Reperfusion Injury
• Malignant Neoplasms
• Retinal Diseases
• Equilibration Disorder
• Glaucoma
• Virus Diseases
• Lung Injury
• Liver Diseases
• Aneurysm
• Neurodegenerative Disorders
• Liver Damage

• Refractory Carcinoma
• Lung Diseases
• Teratocarcinoma
• Inflammatory Response
• Carcinoma
• Lung Diseases, Obstructive
• Chronic Obstructive Airway Disease

Interacting Proteins

• GABARAP
• GABARAPL1
• GABARAPL2
• MAP1LC3A
• MAP1LC3B

• MAP1LC3C

Pathways

• Autophagy
• Cell Death
• Conjugation
• Cellular Homeostasis
• Secretion
• Programmed Cell Death
• Proteolysis
• Equilibrioception
• Phagocytosis
• Catabolic Process
• Rna Interference
• Cellular Process
• Inner Ear Development

• Regulation Of Autophagy
• Membrane Biogenesis
• Inflammatory Response
• Senescence
• Macroautophagy
• Sensitization
• Translation

PTMs

• Cleavage

• Phosphorylation

• Reduction

Research Areas

• Autophagy
• Cancer

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/ATG4B

Best Uses Of The ATG4B Marker

If you've ever wondered what the best use for the ATG4B marker is, this article will help you find out. This particular marker has a lot of applications, including the monitoring of the expression of different cytokines in the human body. It also identifies the presence IL-1a cytokine. If you are interested in learning more about IL-1a and IL-6 as well as IL-10, you can read on.

IL-1a

ATG4B is a member of the Atg gene family. It has four human homologs and seven in other mammals. Both members the ATG gene familial belong to two distinct families, MAP1LC3/LC3 or GABARAP. Atg4B activates LC3B at a rate more than 1500 times greater than its human homolog Atg4A. It is believed to play an important role in autophagosome maturation.

S130 inhibits the ATG4B enzyme, as shown by its inhibition of ATG4B activity. The fitted FRET test curve calculates S130. The yellow dotted lines show hydrogen bonds between S130 and ATG4B. ATG4B was incubated with 10mM S130 for 30 minutes, followed by the addition of FRET–GABARAPL2 (and SDS-PAGE) The enzymes that undergo FRET-cleavage with S130 were detected by SDS-PAGE.

ATG4B has been shown to be important in some experimental models for autophagy regulation. In a study in cancer cells, overexpression of ATG4B increased cell viability when compared to ATG4B-deficient cells. GFP-LC3 puncta accumulate during autophagy in wild type cells. Autophagy can be highly active if ATG4B in cells is missing. This can lead to a cytotoxic effect.

ATG4B has a significant role in cancer biology as well. High-throughput screening techniques can be used to identify new inhibitors. Some inhibitors have been shown to inhibit ATG4B, although most were only tested in vitro. ATG4B is a key component of cancer cell biology. In silico Screening is a powerful way to identify compounds that inhibit the protein.

IL-6

The ATG4B gene regulates the cell cycle and can cause apoptosis. Cells that were previously resistant can now be reverted to their normal state by ATG4B overexpression. ATG4B is vital for cell survival and normal cellular growth.

Overexpression of ATG4B in cells results in enhanced cell viability, even in starvation medium. Moreover, cells with ATG4B overexpression showed higher viability compared to wild-type controls. GFP-LC3 puncta and LC3II puncta accumulates in wild-type cells. S130 suppresses autophagy flux. S130, a hallmark sign of autophagy is also produced when ATG4B is pharmacologically inhibited.

Many researchers have used ATG4B to target cancer therapy. This gene encodes a protein that regulates the ATG4B gene. ATG4B can be considered one of the key transcription factors in cancer. It is essential for the growth of a cell and may even be a target for a new anticancer drug. It is therefore important to find a drug to inhibit ATG4B.

S130 inhibits cancer autophagy and increases apoptosis. Inhibition of S130 decreases autophagy activity and promotes apoptosis. Activated ATG4B significantly rescues cytotoxicity in cancer cells. S130 however, inhibits autophagy.

IL-10

The ATG4B mark is a key regulator in autophagy. It inhibits S130 and is associated with enhanced cytotoxicity. The gene has potential to affect the growth of cancer cells. It is highly toxic and has high activity in both adherent and suspension cells. It is highly selective and inhibits S130, an autophagy-inducing protein.

The ATG4B gene can be found in many tissues and cells of the body. The gene encodes proteins involved in autophagy. ATG4B helps to form LC3II. ATG4B deficiencies can cause LC3II and LC3II to be ineffective. It plays two key roles in autophagy. It promotes LC3 lipidation as well as delipidation. It may lead to a net increase in LC3-II.

ATG4B may also be involved in cell-death. ATG4A/ATG4BC74S is not overexpressed to significantly increase their activity. ATG4B has a specific enzymatic activity. Restoring ATG4B expression partially rescued ATG4-deficient cells with a higher apoptotic level. This caused changes in LC3-I and cleaved CASP3.

ATG4B encodes many important roles in autophagy. This makes it an important target of drug discovery. ATG4B inhibitors must be powerful and effective. To develop an effective drug for this gene, several screening approaches are necessary. Ultimately, we need to understand ATG4B's role in tumorigenesis. This will allow for the design and development of new treatments.

ATG4B inhibitors are small-molecule agents that inhibit ATG4B function. Some were not validated with gel-based testing. This method can overestimate the potency of drugs. In this case, molecular docking and FRET assays can be used to identify ATG4B inhibitors.

S130 is an ATG4B inhibitor that inhibits ATG4B's activity in HeLa cells. This inhibitor inhibits ATG4B cell death. The cells were treated by 10 mM s130, necrostatin-1 or CCASP3.

IL-10, IL-10, IL-10

The ATG4B marker serves multiple functions. It can detect a biomarker for cancer, inflammation, or developmental biology. It also regulates the immune system. Its reduced activity makes cells more susceptible to exogenous stress like starvation. It is unknown how ATG4B promotes and reduces cell survival.

The ATG4B protein is a potential target for anticancer treatment. Studies have shown that S130's binding ability to ATG4B was not affected by Cys74 mutation. This is encouraging news for future anticancer treatments. S130 has also been reported to be highly affinity for ATG4B. It is also highly effective in reducing the growth of cancer cells.

ATG4B is a cysteine protease. It is an important part of macroautophagy. It cleaves Atg8 homologs. It is highly expressed on colorectal and breast cancer cells. Consequently, inhibition of ATG4B may sensitize cancer cells to therapeutic agents. It is important that you identify potent inhibitors in order to further study ATG4B.

Transient expression of ATG4B was evaluated using a gel-based assay. ATG4B efficiently cleaves FRET–GABARAPL2, and this activity could be suppressed with S130, which is a potent inhibitor. ATG4B cleavage activity, which is also important for ATG4B, was also assessed in HeLa cell lines that had ATG4B deleted. The same procedures were followed in transfection of ATG4B from HeLa cells. The cell proteins were evaluated 24 hours after transfection.

The ATG4B marker can be used for research purposes. It can be used for immunocytochemistry and multicolor flow cytometry. For easy conjugation to any of your labels, the antibody can be obtained in carrier-free versions. Its associated products are listed below. It is important for you to know that the ATG4B mark has multiple applications and is not intended as a therapeutic tool.

It has been shown that ATG4B can enhance cell viability in starvation medium. When ATG4B overexpression was compared to the same levels in cells with ATG4B deficiency, cell viability was enhanced. The marker's overexpression led to an increase in the accumulation of LC3II and GFP–LC3 punctas. Autophagy activation can turn into a stress when it is prolonged, and the S130 protein inhibits autophagy.