Cysteine protease ATG4A Antibodies

Cysteine protease ATG4A (ATG4A)

Cysteine protease required for the cytoplasm to vacuole transport (Cvt) and autophagy. Cleaves the C-terminal amino acid of ATG8 family proteins to reveal 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. Preferred substrate is GABARAPL2 followed by MAP1LC3A and GABARAP.

Gene Information

Human
Gene Name:	ATG4A
Uniprot:	Q8WYN0
Entrez:	115201

Family

Belongs to:
peptidase C54 family

Alternative Names

APG4 autophagy 4 homolog A (S. cerevisiae); Apg4a; ATG4 autophagy related 4 homolog A (S. cerevisiae); ATG4A; Atg4al; Autl2; AUT-like 2 cysteine endopeptidase; AUT-like 2, cysteine endopeptidase (S. cerevisiae); Autophagin 2; autophagin-2; cysteine endopeptidase; cysteine protease ATG4A; EC 3.4.22; EC 3.4.22.-; hAPG4A

Molecular Weight

Mass (kDA):
45.378 kDA

Genomic Context

Human
Location:	Xq22.3
Sequence:	X; NC_000023.11 (108091667..108154671)

Tissue Specificity

Widely expressed, at a low level, and the highest expression is observed in skeletal muscle and brain. Also detected in fetal liver.

Subcellular Localizations

Cytoplasm.

Diseases

• Malignant Neoplasms
• Carcinoma
• Neoplasms
• Granuloma
• Crohn Disease
• Neoplasm Metastasis
• Diabetic Ketoacidosis
• Neurodegenerative Disorders
• Malignant Neoplasm Of Breast
• Ataxia
• Intestinal Diseases
• Endoplasmic Reticulum Stress

• Edema
• Tumor Angiogenesis
• Mammary Neoplasms
• Malignant Squamous Cell Neoplasm
• Nerve Degeneration
• Malignant Paraganglionic Neoplasm
• Diabetes Mellitus

Interacting Proteins

• CDKL3
• GABARAPL1

Pathways

• Autophagy
• Cell Death
• Macroautophagy
• Pathogenesis
• Granuloma Formation
• Transport
• Programmed Cell Death
• Autophagic Cell Death
• Angiogenesis

• Rna Interference
• Localization
• Conjugation

PTMs

• Cleavage

• Phosphorylation

• Reduction

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/ATG4A

Best Uses Of The ATG4A Marker

Antibodies that are specific for the ATG4A gene can be a great tool in research, especially when they are used in conjunction with other proteins. There are three main things to consider when purchasing an anti-body: Validation, Specificity, and Applications. We'll be discussing these questions in more detail in this article. Continue reading to learn more about anti-ATG4A markers and their benefits.

Anti-ATG4A Marker

ATG4A has been shown to be required for mammosphere creation in studies. ATG4A overexpression significantly increases sphere formation, but decreases the level of mRNA. After expression of both shRNAs, the mRNA levels were lower. To determine the mechanism of ATG4A gene overexpression, the shRNA sequences from both shRNAs were cloned in expression vectors.

ATG4A regulates autophagy via JakSTAT signalling. Autophagy involves the destruction of damaged organelles and macromolecules by cells. Autophagy has been linked to breast-cancer stem cell maintenance. The inhibition of ATG4A prevented the proliferation of cancer-stem cells. It also inhibited f1Fo ATP synthase activity in HCC cells.

Boster provides antibodies that have high affinity. They have been widely cited in the scientific community over the past twenty-five years and have been validated on immunohistochemistry, Western Blotting, and ELISA. These antibodies are extremely relevant to research and are trusted worldwide by scientists. All Boster antibodies have been tested on multiple platforms for high affinity and specificity. Boster is a good choice if you are looking for an antibody that can study ATG4A.

ATG4A expression regulates formation of mammospheres within breast cancer cell lines. It regulates breast cancer cell growth under physiological conditions. We tested this by injecting these cells into NSG mouse models. The formation and spread of tumours in MDAMB-231- and luminal MCF-7 cellular cells was significantly increased by ATG4A. The burden of tumours was significantly reduced by knocking down ATG4A.

The Anti -ATG4A Marker found in the Boster Biologic catalog is available to be used for research in ELISA (IHC-P), and WB. The Antibody was raised to a specific 18 amino-acid peptide. This corresponds roughly to the last fifty ATG4A amino acid sequences. Boster Bio Antibodies sells longer blocking peptides.

Applications

The ATG4A marker recognizes endogenous ATG4A. It is a member to the C54 family of cysteine proteaseases. It has been extracted from human cytosol through immunogen and affinity purification. Autophagy is a biological process where cells destroy unneeded and damaged organelles and proteins to maintain their integrity. Malignant tumors have lower levels of autophagy, which indicates a role for this protein in unregulated cell death and growth.

One study found that miR-24-3p in H446 cell cultures could induce ATG4A. Upon co-transfection of the cells with either miR-24-3p, autophagy was inhibited. Autophagy was inhibited by knocking down ATG4A. These results have important implications in the field autophagy.

ATG4A promotes breast cancer stem-like and mammosphere formation. It is responsible for organelle clearance during differentiation as well as autophagosome maturation. It targets the autophagosome membranes and cleaves human light chains 3/MAP1LC3B at Met121. Therefore, the ATG4A marker has several applications. It is possible to identify cancer stem cells if you have the ATG4A protein or gene.

Autophagy is a complex process in cells that occurs when the autophagy related gene (ATG), proteins catalyze autophagy. ATG4A is one of the ATG4A peptidases. It is a 398-amino-acid protein. It acts as a cysteine protease and cleaves MAP1LC3 from its C-terminus. N-ethylmaleimide can inhibit Atg4A.

Specificity

A biochemical reporter test was used to determine ATG4A's specificity. Mixing 100 nM GATE16-PLA2 with recombinant ATG4B was enough to produce fluorescence intensity of 1 h.

ATG4A, also known to be autophagy related proteins 4 homolog A or (ATG4A), a 50kDa cytosolic cycleine protease. Autophagy refers to a biological process in which damaged or endogenous protein are destroyed by the body. The human ATG4A Gene shares 94% homology (with the genes from mouse, chimpanzees or dog)

The ATG4B proteins can be found in two forms: the closed and open. The open form contains a tail at its N-terminus that binds LC3. The C-terminal area of the closed form is located within the active site. The Trp142 molecule is in close contact to Pro260 and prevents the LC3 interacting with ATG4B.

The ATG4A gene is expressed on a cell surface and is located in the cytoplasm, where it is important to regulate the activity of the ATG4A protein. ATG4A inhibitors were chosen based on their ability inhibit caspase-3. In vitro, inhibitors against ATG4A could be tested in HCT116 and H4 cells as well as MDA-MB-231 mice. Positive controls were Doxorubicin and DMEM.

The immunoblotting of cells transfected in with HA-tagged ATG4 member cells confirmed that siRNA targeting ATG4 had a knockdown effect. The mean + SEM of three independent experiments are used to report the results. If the ATG4B gene was deleted after HER2 expression was decreased, the results were significant. These results indicate that ATG4B is required to ensure cell survival in HER2-overexpressing cancer cells.

Validation

ATG4A is a positive regulator of autophagy, a cell-degradation pathway that removes damaged organelles and macromolecules from the cell. The maintenance of cancer stem-like cell types is affected by this gene. The marker is redoxregulated and inhibits an activity of a lymphosome. Autophagy promotes maintenance of a stem-like phenotype within breast cancer cells.

ATG4A expression is also found in a variety cancers, including breast carcinoma. In humans, the gene is often expressed in high levels in tumourigenesis cells. This activity increases the risk for developing aggressive tumors in mice. The gene can be used in order to identify cancer cells carrying the gene. It can also promote tumour growth by being associated with inflammation processes. The Boster bio platform is easy to use, and its validation is pending.

Boster Bio's ATG4A antigen antibody reacts to both mouse and human protein. This antibody can be used in Western Blotting, IP, and ELISA. The antibody can be purchased in Liquid Form. It can be purchased in the Boster Bio catalog #A06539-1. The antibody can be stored at -20degC for one year. Further, the antibody is suitable for use with human and mouse cells.

ATG4B inhibition reduces the growth of cancer cells. In order for inhibitors to be effective in the body they must be capable of inhibiting autophagy. To understand the complex crosstalk between ATG4B activation and cell death, more research is needed. ATG4A is the most widely used biomarker in Boster Bio. Its availability is the key for discovering new drugs in future.

Refer to

The ATG4A cell surface marker is important in gastric cancer. It regulates EMT (stemness) in gastric tumor cells via the Notch Signaling pathway. However, the ATG4A gene does not regulate autophagy. This article will review the literature on ATG4A, and the role it plays for gastric cancer. ATG4A has been described as a potential marker of gastric cancer since the early 1990s.

ATG4A, a cysteine protein that is involved in Notch signaling, is known as ATG4A. In NSG mice, the risk for developing aggressive tumors increases if this protein is overexpressed. This gene is also involved with other diseases. To confirm the significance and role of ATG4A in CML, genetic testing is required. It could also be linked to susceptibility for drugs. It is also the target of drug discovery for CML stem cell drugs.

There are many possible genetic variations of the ATG4A marker. Studies show that some of them are associated with cervical cancer. ATG4ASNPs are among those that are associated with HPV infections. This association, although not conclusive in its entirety, supports the hypothesis ATG4A might be associated with cervical carcinoma. This new evidence relates to the association between ATG4A and cervical cancer.

While it is well-known that the ATG4A genome is involved in autophagy processes, it is not clear how it regulates gene gene expression. Numerous studies have suggested that ATG4A could be correlated and affected by SNPs. This may affect gene transcription and function. SNPs can also affect ATG4A. These variations could indirectly affect the expression. This is why ATG4A is so important and how it plays a role in autophagy.