The BST1 Chimeric Recombinant Rabbit Monoclonal Antibody (HDAB0282) is a powerful tool for research involving BST1, a cell surface molecule with implications in immune function and inflammation regulation. This antibody, developed using cutting-edge technology, exhibits high specificity and sensitivity towards human BST1 protein samples, making it a reliable choice for Western blot applications.BST1, also known as bone marrow stromal antigen 1, is involved in modulating immune responses and has been linked to various diseases, including autoimmune disorders and inflammation-related conditions.
By targeting BST1 with this monoclonal antibody, researchers can gain insights into its function and potential therapeutic implications in cancer research and immunology studies.By utilizing the BST1 Chimeric Recombinant Rabbit Monoclonal Antibody, researchers can enhance their understanding of BST1's role in immune regulation and disease progression, ultimately contributing to the development of novel treatments and interventions in the field of biomedicine.
SKU:
HDAB0282
Size:
100 µg
Clonality:
Monoclonal
Clone:
DMC444
Synonyms:
CD157
Applications:
Flow Cyt
Recommended Dilution:
Flow Cyt 1:100
Host Species:
Rabbit
Isotype:
Rabbit/Human Fc chimeric IgG1
Reactivity:
Human
Purification Method:
Purified from cell culture supernatant by affinity chromatography
Formulation:
Powder
Buffer:
1XPBS
Storage:
Store at -20°C to -80°C for 12 months in lyophilized form. After reconstitution, if not intended for use within a month, aliquot and store at -80°C (Avoid repeated freezing and thawing).Lyophilized antibodies are shipped at ambient temperature.
Usage:
Research use only
Background:
Bone marrow stromal cell antigen-1 is a stromal cell line-derived glycosylphosphatidylinositol-anchored molecule that facilitates pre-B-cell growth. The deduced amino acid sequence exhibits 33% similarity with CD38. BST1 expression is enhanced in bone marrow stromal cell lines derived from patients with rheumatoid arthritis. The polyclonal B-cell abnormalities in rheumatoid arthritis may be, at least in part, attributed to BST1 overexpression in the stromal cell population.
