R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
LGALS3BP (F2K6Q) Rabbit mAb #38514
Filter:
- WB
Supporting Data
REACTIVITY | H M R |
SENSITIVITY | Endogenous |
MW (kDa) | 100, 75-80, 28 |
Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
Product Information
Product Usage Information
Application | Dilution |
---|---|
Western Blotting | 1:1000 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/mL BSA, 50% glycerol, and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
LGALS3BP F2K6Q) Rabbit mAb recognizes endogenous levels of total LGALS3BP protein. This antibody reacts with proteins running at 100kDa, 75-80kDa, and 28kDa. These proteins are likely cleavage products of full-length protein.
Species Reactivity:
Human, Mouse, Rat
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly152 of human LGALS3BP protein.
Background
LGALS3BP is a complex, hyperglycosylated, secreted protein that is involved in regulating a number of important biological processes. These include cell signaling and adhesion, migration, proliferation, and potentially immune response regulation via natural killer cell function (1,2,3). Upon secretion of LGALS3BP into the extracellular matrix (ECM), it interacts with galectins, such as LGALS-3, and ECM components, such as fibrinogen and collagen, as well as members of the integrin family (4). LGALS3BP binding to LGALS-3 modulates LGALS-3 activity and results in downstream changes in cell-cell and cell-matrix interactions (1).
Essentially, LGALS3BP-mediated integrin activation triggers intracellular signaling pathways, including the Akt, JNK, and Ras-ERK cascades. These pathways are essential for cell proliferation and survival. Essentially, LGALS3BP can activate signaling pathways that promote cell growth. Not surprisingly, therefore, LGALS3BP is overexpressed in certain pathological conditions, notably in various cancers, including pancreatic, lung, and breast cancers, hepatocellular carcinoma, and other tumor types. (3-6). Overexpression is associated with tumor progression, metastasis, and poor prognosis (5). It plays a role in other disease conditions, such as hepatic fibrosis, where it influences TGF-β1 signaling and availability, viral infections, such as HIV, and autoimmune diseases, such as systemic lupus erythematosus (2-7).
LGALS3BP is a multifaceted protein with significant roles in cell biology and disease. Its involvement in cancer progression and other pathological conditions makes it an area of active research, and overexpression in tumors makes it a promising target for diagnostic antibodies and drug development (4,8,9).
Essentially, LGALS3BP-mediated integrin activation triggers intracellular signaling pathways, including the Akt, JNK, and Ras-ERK cascades. These pathways are essential for cell proliferation and survival. Essentially, LGALS3BP can activate signaling pathways that promote cell growth. Not surprisingly, therefore, LGALS3BP is overexpressed in certain pathological conditions, notably in various cancers, including pancreatic, lung, and breast cancers, hepatocellular carcinoma, and other tumor types. (3-6). Overexpression is associated with tumor progression, metastasis, and poor prognosis (5). It plays a role in other disease conditions, such as hepatic fibrosis, where it influences TGF-β1 signaling and availability, viral infections, such as HIV, and autoimmune diseases, such as systemic lupus erythematosus (2-7).
LGALS3BP is a multifaceted protein with significant roles in cell biology and disease. Its involvement in cancer progression and other pathological conditions makes it an area of active research, and overexpression in tumors makes it a promising target for diagnostic antibodies and drug development (4,8,9).
- White, M.J. et al. (2015) J Immunol 195, 1858-67.
- Zhang, X. et al. (2019) Cell Signal 63, 109359.
- Xu, G. et al. (2019) PLoS Pathog 15, e1008002.
- Capone, E. et al. (2021) J Transl Med 19, 405.
- Kim, D.H. et al. (2024) Cancer Commun (Lond) 44, 1106-1129.
- El Bannoudi, H. et al. (2023) Arthritis Rheumatol 75, 711-722.
- Choi, Y.S. et al. (2022) Proc Natl Acad Sci U S A 119, e2119048119.
- Li, L. et al. (2024) Aging (Albany NY) 16, 4033-4051.
- Dufrusine, B. et al. (2023) Mol Oncol 17, 1460-1473.
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