BAX (3-16) Mouse Monoclonal Antibody [Clone ID: 2D2]

Specifications

Product Data
Clone Name	2D2
Applications	FC, IF, IHC, IP, WB
Recommend Dilution	ELISA: Use Free BSA Antibody for coating. Western Blot: 0.5-1 µg/ml. Flow Cytometry: 0.5-1 µg/106 cells. Imunoprecipitation: 1-2 µg/500 µg protein lysate. Immunofluorescence: 1-2 µg/ml. Immunohistochemistry on Frozen and FormalinFixed Paraffin Sections: 0.5-1 µg/ml for 30 minutes at RT. Staining of formalin-fixed tissues requires boiling tissue sections in 1mM EDTA buffer, pH 7.5-8.5, for 10-20 min followed by cooling at RT for 20 minutes. Positive Control: Jurkat, K562, HL-60, or HeLa Cells. Reed-Sternberg cells in Hodgkin’s lymphoma.
Reactivity	Human, Monkey
Host	Mouse
Clonality	Monoclonal
Immunogen	A synthetic peptide corresponding to Amino acids 3-16 of Human Bax protein
Specificity	Recognizes a protein of 21kDa, identified as the Bax protein. This Monoclonal Antibody is highly specific to Bax and does not cross react with bcl-2 alpha or bcl-X protein. Cellular Localization: Cytoplasmic. Negative Species: Mouse and Rat.
Formulation	10mM PBS State: Purified State: Liquid purified IgG fraction from Bioreactor Concentrate Stabilizer: 0.05% BSA Preservative: 0.05% Sodium Azide
Concentration	lot specific
Purification	Affinity Chromatography on Protein A/G
Conjugation	Unconjugated
Storage Condition	Store undiluted at 2-8°C.
Predicted Protein Size	21 kDa
Gene Name	BCL2 associated X protein
Database Link	Entrez Gene 718948 MonkeyEntrez Gene 581 Human UniProt ID Q07812
Background	The human protein Bax sits at a critical regulatory junction of apoptosis, or programmed cell death. Activated Bax changes conformation, inserts into the MOM (Mitochondrial Outer Membrane), oligomerizes, and induces MOM permeabilization, causing the release of cytochrome c, which effectively commits the cell to die. (Ma J et al., 2012). Mechanisms of membrane perforation include formation of hetero-oligomeric complexes of Bax with other pro-apoptotic proteins such as Bak, or formation of lipidic pores physically aided by mitochondrial membrane-inserted proteins (Garg P et al., 2012). Connexins play important roles in many physiological and pathological processes. In the context of apoptosis, Cx43 translocated to the mitochondria, where it interacted with Bax to initiate the mitochondrial apoptotic pathway. The 241-382 aa region of Cx43 was required for interaction with Bax. Furthermore, this region was responsible for permeabilizing mitochondrial membrane potential. Recent studies elucidate a novel mechanism of the Cx43-mediated regulation of apoptosis in pancreatic cancer (Sun Y et al., 2012). Bax acts as a biomarker that exhibited a difference in sub-cellular localization between normal OCSE (Oral Cavity Squamous Epithelium) and OSCC (Oral Cavity Squamous Cell Carcinoma) and was also the only apoptotic protein significantly associated with prognosis. The translocation of Bax from the nucleus to the cytoplasm in OSCC is consistent with increased Bax function at the mitochondria, leading to improved sensitivity to radiotherapy-induced apoptosis in tumours with elevated Bax expression. Bax antibody can be used to study the intracellular redistribution of Bax protein upon induction of apoptosis and its unique subcellular localization. This product can also be used in immunoblot analysis to estimate variations in the expression of specific proteins involved in apoptosis signaling (Bose P et al., 2012).
Synonyms	Apoptosis regulator BAX, BCL2L4, Bcl2-L-4
Reference Data
Protein Families	Druggable Genome, Transmembrane
Protein Pathways	Amyotrophic lateral sclerosis (ALS), Apoptosis, Colorectal cancer, Huntington's disease, Neurotrophin signaling pathway, p53 signaling pathway, Pathways in cancer, Prion diseases

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