Apoptosis regulator Bcl-2 Antibodies

Apoptosis regulator Bcl-2 (BCL2)

Suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. Regulates cell death by controlling the mitochondrial membrane permeability.

Appears to function in a feedback loop system with caspases. Inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria or by binding to the apoptosis-activating variable (APAF-1).

Gene Information

Human
Gene Name:	BCL2
Uniprot:	P10415
Entrez:	596

Family

Belongs to:
Bcl-2 family

Alternative Names

apoptosis regulator Bcl-2; B-cell CLL/lymphoma 2; Bcl2; Bcl-2

Molecular Weight

Mass (kDA):
26.266 kDA

Genomic Context

Human
Location:	18q21.33
Sequence:	18; NC_000018.10 (63123346..63320280, complement)

Tissue Specificity

Expressed in a variety of tissues.

Subcellular Localizations

Mitochondrion outer membrane; Single-pass membrane protein. Nucleus membrane; Single-pass membrane protein. Endoplasmic reticulum membrane; Single-pass membrane protein.

Diseases

• Neoplasms
• Malignant Neoplasms
• Lymphoma
• B-cell Lymphomas
• Carcinoma
• Leukemia
• Lymphoma, Follicular
• Diffuse Large B-cell Lymphoma
• Chromosomal Translocation
• Malignant Paraganglionic Neoplasm
• Malignant Neoplasm Of Breast
• Mammary Neoplasms

• Cell Transformation, Neoplastic
• Lymphoma, Non-hodgkin
• Neoplasm Metastasis
• Chronic Lymphocytic Leukemia
• Lymphoid Leukemia
• Cytogenetic Abnormality
• Myeloid Leukemia

Interacting Proteins

• AMBRA1
• BAD
• Bad
• BAK1
• BAX

• BBC3
• BCAP31
• BCL2L11
• BCLAF1
• BECN1

• BID
• BIK
• Bmf
• BNIP3L
• BRCA1

• CISD2
• Itpr1
• LRRK2
• MDM4
• NLRP1

• NR4A1
• PMAIP1
• SIVA1
• TP53
• TP53BP2

Pathways

• Cell Death
• Cell Cycle
• Cell Proliferation
• Pathogenesis
• Induction Of Apoptosis
• Cell Growth
• Programmed Cell Death
• Cell Cycle Arrest
• Localization
• Interphase
• Autophagy
• Angiogenesis
• Methylation

• Aging
• Cell Differentiation
• Drug Resistance
• Dna Repair
• Translation
• Secretion
• Immune Response

PTMs

• Phosphorylation
• Cleavage
• Methylation
• Dephosphorylation
• Reduction
• Oxidation
• Acetylation
• Phosphorothioation
• Ubiquitination

• Demethylation
• Deacetylation
• Glycosylation
• Carboxylation
• Decarboxylation
• Phosphorothionation
• Citrullination
• Acylation
• Amination

• Deglycosylation

Research Areas

• Apoptosis
• Autophagy
• Cancer
• Tumor Suppressors

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/BCL2

Best Uses of the BCL2 Marker

The BCL2 marker is an anti-cancer antibody that has been documented to have many applications. This protein is utilized in cancer screening to differentiate basal cell carcinoma from squamous cell carcinoma. Additionally, it stimulates cell Apoptosis and is stored at temperatures of -80° C. This article will discuss the best applications for this marker. Continue reading to learn more. Boster Bio The Best Uses for the BCL2Marker

Anti-Bcl-2 antibody is an established cancer marker

BCL-2 is a protein that is expressed in many different types of leukemias and other types of hemopoietic cells. The amount of BCL-2 is dependent on the population of cells and the stage of maturation or activation. In a leukemic line model, BCL-2 expression is higher than control cells with or without translocation. The expression of BCL-2 can be a biomarker for the presence of cancer.

BCL-2 family proteins include pro-apoptotic and anti-apoptotic proteins. The main member of this family, BCL-2, is distinguished by the presence of four BCL-2 homologydomains. The Bcl-2 family members that are anti-apoptotic have been linked to the chemoresistance of various forms of human cancer. There are currently several experimental drugs that target this protein in clinical trials.

BCL-2 family proteins are essential regulators of the mitochondrial apoptotic pathway. In addition to regulating apoptosis and apoptosis, treatments targeting BCL-2 have shown clinical efficacy in B-cell malignancies. Patients with advanced B-cell malignancies have observed significant clinical activity for treatments that target BCL-2. Additionally, cancer cells acquire resistance to inhibition of BCL-2 because of metabolic adaptation and dysregulated cellular energy. To overcome resistance to drugs the BCL-2 family of protein inhibitors that target metabolism deregulated are being investigated.

Anti-BCL-2 antibodies are useful as a cancer indicator for a variety of reasons. It helps doctors choose patients based on the resistance of tumor cells the drug. Anti-BCL-2 antibodies are also used to identify patients in the beginning stages of cancer and relapse. It is important to understand the clinical significance of Anti-Bcl-2 antibodies as a prognostic indicator.

It is used to distinguish basal cell carcinoma from other cancers of the squamous.

Boster Bio's BCL2 marker has been found to differentiate basal cell carcinoma from squamuous cancers. This gene is present in both squamous and basal cells. BCL2 expression was significantly higher in basal cells than in Squamous cancers. APC and CK7 were also more prevalent in stages IA tumors than in the squamous cell.

These markers are associated with cell apoptosis. They were associated with PTEN and p-AKT. They were decreased in U251/MDR cell lines. Furthermore, LRIG1 expression was decreased in U251/MDR cells while BCL-2 expression was elevated in the BA/lepidic pattern. However, this does not mean that BCL2 is an accurate predictor of tumor reaction to chemotherapy and recurrence.

It is believed to promote cell death.

Cisplatin kills cells by binding to the HDAC death receptor. In this study, Linc00312 siRNA inhibited apoptosis in K562 cells. The GV146 NC group had the most powerful effect. The SKOV3 SKOV3 group had most minimal effect. The Linc00312 siRNA blocked apoptosis in an dose-dependent manner.

Another study revealed that a protein known as ILKAP plays a role in the death of cells. It was identified as serine/threonine-phosphatase in 1998. It is a member of the protein phosphatase 2C family and binds directly to the outer mitochondrial membrane. ILKAP induces cell death and blocks downstream signaling pathways.

For prolonged hypoxia-induced apoptosis, ILKAP is required. Ad-ILKAP decreased cell viability and activating apoptosis markers. ILKAP also reduced levels of HIF-1a in a dose-dependent manner. Western blotting revealed that HIF-1a levels increased after 48 hours, however it decreased when hypoxia is prolonged. The results also revealed that ILKAP blocks TUNEL activation and is which is a TUNEL assay.

It is not specific for the follicular lymphoma

Follicular lymphoma, which is afflicting approximately one in five Americans is a very common type of cancer. It grows slowly but some cases can be extremely dangerous. This type of cancer can lead to an involuntary swelling of the lymph nodes, generalized aches, and discomfort. Follicular lymphoma can be difficult to treat and may develop into non-Hodgkin lymphoma large B-cell lymphoma diffuse, or more aggressive forms.

The chance of follicular lymphoma transformation is extremely high. It affects two to three percent patients every year. Patients with high-grade lymphoma as well as those with underlying low-grade lymphoma are at greater risk. The immunohistochemical profile of every patient is vital in the initial pathologic examination. It aids in predicting the outcome. About a quarter of patients with transformed follicular lymphoma will develop high-grade B-cell lymphoma.

The World Health Organization (WHO) is a classification system for disease entities according to their morphologic features as well as their immunologic features and genetic constitution, as well as their clinical behavior, and behavior. Follicular lymphoma could be considered an archetype. Most cases of the disease have the same morphologic characteristics, which include the t(14-18) translocation of the chromosome. There are some exceptions to this rule however. This is why a correct classification is essential for understanding the entire diagnostic spectrum of follicular lymphoma.

Fortunately, a new test has revealed another clone which has the same molecular structure in high and low-grade Follicular lymphoma. Next-generation sequencing of the immunoglobulin variable region showed that t(14;18) or BCL2/IGH rearrangement occurred in high-grade lymphoma patients. However, a biopsy remains required to establish the diagnosis and determine the severity of the disease.