Bms-1166
Bms-1166 - Related Videos
03:27
2D Co-culture of Leukemic Cells with BMSCs: A Method to Obtain Subpopulations of Leukemic Cells
0 Views •
2023
This video describes the technique for long term 2D co-culture of leukemia cells with bone marrow stromal cells to study their interaction with the bone marrow microenvironment. The 2D coculture model utilizes the acute lymphoblastic leukemia cells and the bone marrow stromal or osteoblasts that influence tumor cell phenotype. This study will support investigation of the mechanisms that underlie bone marrow supported survival of leukemic cells during chemotherapy exposure.
04:00
Isolation and Culture of Bone Marrow Stromal Cells from a Mouse Tibia
0 Views •
2025
In this video, we demonstrate the isolation and culture of bone marrow stromal cells from the long bones of mice. The isolated adherent BMSCs can be used for further analysis.
03:03
In Vitro Mouse Bone Marrow Stromal Cell Differentiation into Adipocytes
0 Views •
2025
This video demonstrates the differentiation of bone marrow stromal cells (BMSCs) into adipocytes. In the two-step process, in the presence of specific growth factors and hormones, undifferentiated BMSCs first differentiate into preadipocytes. The second step involving treatment with glucose and insulin leads to the formation of mature adipocytes with multiple lipid droplets.
09:05
In Vitro Differentiation of Human Mesenchymal Stem Cells into Functional Cardiomyocyte-like Cells
0 Views •
Cited by 62 •
2017
Here, we present a method to efficiently harness the cardiac differentiation potential of young sources of human mesenchymal stem cells in order to generate functional, contracting, cardiomyocyte-like cells in vitro.
09:34
Preparation of Plasma Membrane Vesicles from Bone Marrow Mesenchymal Stem Cells for Potential Cytoplasm Replacement Therapy
0 Views •
Cited by 10 •
2017
Age-related diseases are associated with multiple defects in components of the cytoplasm. Here, we present a protocol to prepare plasma membrane vesicles from bone marrow mesenchymal stem cells. This technique could potentially be used as a means of cytoplasm replacement therapy to ameliorate or even reverse age-associated phenotypes.
FAQs
Dimerization provides a mechanistic link between compound binding and checkpoint disruption. By promoting association between PD-L1 molecules at the protein interface, BMS-1166 changes the availability of the surface involved in PD-1 recognition. This makes dimerization an experimentally useful feature for connecting molecular binding events with reduced checkpoint signaling in tumor-related immune studies.
The hydrophobic pocket serves as the binding site that positions BMS-1166 at the PD-L1 interface. Occupying this pocket is important because it supports the structural change associated with PD-L1 dimerization and limits productive PD-1 engagement. Studies of this interaction help clarify how a small molecule can modulate a protein-protein checkpoint interface.
BMS-1166 can help researchers separate checkpoint-mediated suppression from other influences on T-cell behavior. When the compound disrupts PD-1 engagement with PD-L1, investigators can examine resulting changes in T-cell responses within an experimental system. These observations provide mechanistic evidence about how the PD-1/PD-L1 interaction contributes to immune regulation in tumors.
As a chemical probe, BMS-1166 is applied to test the consequences of selectively modulating PD-L1 rather than treating the checkpoint pathway as an unexamined target. Researchers can use it to investigate PD-1/PD-L1 signaling, monitor T-cell responses, and evaluate whether experimental checkpoint blockade produces effects relevant to anticancer research.
Studies can assess whether disrupting the PD-1/PD-L1 interaction is accompanied by changes in T-cell activity or other measured immune responses in a cancer-research model. The compound therefore connects molecular mechanism to functional outcome. Interpreting those results can indicate how strongly checkpoint modulation contributes to the response observed under the tested conditions.
The comparison helps define what small-molecule PD-L1 modulation contributes beyond established antibody-based approaches. BMS-1166 offers a chemical strategy for probing the same checkpoint relationship and can be examined in experimental combination settings. Such work may clarify whether small-molecule modulation complements antibody immunotherapy and informs the design of investigational anticancer treatments.