Cell Adhesion
This critical biological mechanism facilitates tissue formation, organ development, and cellular signaling.
It involves complex interactions between cell surface receptors, adhesion molecules, and the cytoskeletal network.
Dysregulation of cell adhesion has been implicated in various pathological conditions, including cancer metastasis, inflammation, and autoimmune disorders.
Researchers in cell biology, tissue engineering, and regenerative medicine actively study cell adhesion to develop novel therapeutic interventions and optimize experimental protocols.
Leveraging the power of AI-driven platforms like PubCompare.ai can help scientists effiiciently locate, compare, and optimize cell adhesion techniques, boosting research productivity and reproducibility.
Most cited protocols related to «Cell Adhesion»
Most recents protocols related to «Cell Adhesion»
Example 8
Cell adhesion was also evaluated by means of in vitro scratch wound-healing assay. HDPSCs cells were analyzed by difference in staining with phalloidin (cell nucleus) and DAPI to visualize actin cytoskeleton.
Cell adhesion results showed excellent interaction and adhesion between neighboring cells in the presence of bioceramic composition. The Bioceramic composition sealer (CB5) and Bioceramic composition repair (CB6), showed a gradual increase in growth over time, an extended morphology and a high content of F-Actin (cell microfilamen), reaching confluence after 72 hours of culture.
The analysis of cell proliferation (via cell viability study), apoptosis, cell adhesion and morphology (via cell adhesion study) and migration (via cell migration study) showed very positive results, indicating that the proposed bioceramic composition induces the odonto/osteogenic mineralization and differentiation process in the presence of tooth-specific human stem cells (hDPSCs pulp). While a market resin sealer was also used in the comparative studies, however, all results were not satisfactory for this product.
Example 5
In order to compare levels of adherence to HEp-2 epithelial cells in culture, we used an established model for evaluating adherence of EHEC O157:H7 (27). HEp-2, human laryngeal carcinoma epithelial cells, were a kind gift from Dr. Carlton Gyles (Department of Pathobiology, University of Guelph). Briefly, HEp-2 cells grown in EMEM supplemented with 10% (v/v) FBS were plated onto 24-well tissue culture plates at 2×105 cells ml−1 and incubated for 24 h in the presence of 5% CO2. The cells were then maintained during the assay in serum and antibiotic-free EMEM. Before inoculation with bacteria, 10% (v/v) of L. acidophilus CFSM selected fractions were added in triplicate to treatment group wells. Wells containing the negative control groups were inoculated with 105 E. coli O157:H7 strain VS94 with or without supplementation with 100 μM propanolol (Sigma-Aldrich Canada Ltd.). Following inoculation of 105 EHEC O157 into treatment and control group wells, the plates were incubated for 3 h at 37° C. in the presence of 5% CO2. The cell monolayers were then washed three times with PBS to remove non-adhering bacteria and fresh medium was added. Cells were incubated for another 3 h and then washed six times with PBS. Washed cells were lysed with 0.1% Triton X-100. Released bacteria present in the suspension were collected and appropriate dilutions were plated on LB agar. To evaluate if the percentage of adherence in the treatment groups was significantly different from that of the control group, where the recovered counts from the control group (2.2×107 CFU ml−1) were considered to be 100%, the percentage of adherence in the negative control and treatment groups were calculated using the following equation.
Example 3
The phenotype did not depend specifically on the RasC/TORC2 or PI3K pathways. Rather, signals from multiple pathways impinging on the cytoskeleton can be integrated to generate the phenotype. RAM (Regulator of Adhesion and Motility) mutants were isolated in a screen for regulators of cell morphology and migration. Mutant cells were more spread and adhered more strongly than wild-type cells. Most of the mutants also displayed strong defects in cell motility and chemotaxis. When constitutively active RasCQ62L was expressed in the RAM mutants, these cells also formed extremely spread cells like those seen in the pten− cell background (
Example 10
Myc encodes a helix-loop-helix transcription factor upregulated in 50-80% of human cancers and is associated with 100,000 US cancer deaths per year. Myc heterodimerizes with its partner Max to control target gene transcription and is deeply integrated into the regulatory and control mechanisms governing cell viability and proliferation. A recent estimate suggests that Myc binds to approximately 25,000 regions in the human genome. The loss of Myc proteins inhibits cell proliferation and growth, accelerates differentiation, increases cell adhesion, and accentuates the response to DNA damage.
We believe that Myc is an ideal target for anti-cancer therapeutics, particularly MM in which it is highly overexpressed by selective disruptive interference of Myc-Max dimerization while permiting Myc-Mad interactions.