Target type: biologicalprocess
The characteristic movement of a cell from the dorsal ridge of the neural tube towards the heart and that contributes to heart formation. [GOC:mtg_heart]
Neural crest cells (NCCs) are a transient population of multipotent cells that arise from the dorsal neural tube during vertebrate embryogenesis. These cells undergo extensive migration, contributing to a wide range of tissues and organs, including the heart. NCC migration during heart development is a complex process involving intricate signaling pathways and interactions with the surrounding environment.
The journey of NCCs from the neural tube to the heart involves several key steps:
1. **Delamination and Epithelial-to-Mesenchymal Transition (EMT):** NCCs detach from the dorsal neural tube, undergoing a transformation from an epithelial state to a mesenchymal state. This transition is characterized by changes in cell adhesion, cytoskeletal reorganization, and increased motility.
2. **Migration Pathways:** NCCs follow specific migratory pathways guided by chemoattractant and chemorepellent signals. These signals include factors like fibroblast growth factors (FGFs), bone morphogenetic proteins (BMPs), and Wnt proteins, which influence NCC directionality and speed.
3. **Cell-Cell Interactions:** NCCs interact with each other and with surrounding cells, contributing to their collective migration and proper positioning. These interactions involve cell adhesion molecules like cadherins and integrins, as well as signaling pathways that promote or inhibit cell movement.
4. **Differentiation into Cardiac Progenitors:** Once NCCs reach the developing heart, they differentiate into various cardiac cell types, including smooth muscle cells, fibroblasts, and Schwann cells. These cells play crucial roles in the formation and function of the heart.
5. **Formation of the Cardiac Outflow Tract:** NCCs contribute significantly to the formation of the outflow tract (OFT), the region connecting the heart to the aorta and pulmonary trunk. NCCs differentiate into smooth muscle cells, contributing to the constriction and dilation of the OFT, regulating blood flow.
6. **Regulation of Heart Development:** NCCs not only contribute to heart structure but also influence its function. They secrete factors like growth factors and neurotransmitters that can regulate heart development and function.
Overall, NCC migration during heart formation is a finely regulated process, essential for proper heart development and function. Defects in NCC migration can lead to congenital heart defects (CHDs), highlighting the importance of understanding this intricate process for both normal development and the treatment of CHDs.'
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| Protein | Definition | Taxonomy |
|---|---|---|
| Folate receptor alpha | A folate receptor alpha that is encoded in the genome of human. [PRO:DNx, UniProtKB:P15328] | Homo sapiens (human) |
| Compound | Definition | Classes | Roles |
|---|---|---|---|
| methotrexate | dicarboxylic acid; monocarboxylic acid amide; pteridines | abortifacient; antimetabolite; antineoplastic agent; antirheumatic drug; dermatologic drug; DNA synthesis inhibitor; EC 1.5.1.3 (dihydrofolate reductase) inhibitor; immunosuppressive agent | |
| 10-propargyl-10-deazaaminopterin | 10-propargyl-10-deazaaminopterin: structure in first source pralatrexate : A pteridine that is the N-4-[1-(2,4-diaminopteridin-6-yl)pent-4-yn-2-yl]benzoyl derivative of L-glutamic acid. Used for treatment of Peripheral T-Cell Lymphoma, an aggressive form of non-Hodgkins lymphoma. | N-acyl-L-glutamic acid; pteridines; terminal acetylenic compound | antimetabolite; antineoplastic agent; EC 1.5.1.3 (dihydrofolate reductase) inhibitor |
| raltitrexed | N-acyl-amino acid | ||
| pemetrexed | pemetrexed disodium : An organic sodium salt that is the disodium salt of N-{4-[2-(2-amino-4-oxo-4,7-dihydro-1H-pyrrolo[2,3-d]pyrimidin-5-yl)ethyl]benzoyl}-L-glutamic acid. Inhibits thymidylate synthase (TS), 421 dihydrofolate reductase (DHFR), and glycinamide ribonucleotide formyltransferase (GARFT). | N-acyl-L-glutamic acid; pyrrolopyrimidine | antimetabolite; antineoplastic agent; EC 1.5.1.3 (dihydrofolate reductase) inhibitor; EC 2.1.1.45 (thymidylate synthase) inhibitor; EC 2.1.2.2 (phosphoribosylglycinamide formyltransferase) inhibitor |