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In 1968 Shirley Chisholm became the first Black woman elected to the United States Congress. In 1972 she launched a campaign for the Democratic presidential nomination, breaking another political barrier.
MORE →Reflects the personal views, recollections, and perspective of the author, Mike Davis.
This is a personal recollection on the Move fire on May 13, 1985
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| Aliases | NCAM1, CD56, MSK39, NCAM, neural cell adhesion molecule 1 | |||||||||||||||||||||||||||||||||||||||||||||||||||||
| External IDs | OMIM: 116930; MGI: 97281; GeneCards: NCAM1 | |||||||||||||||||||||||||||||||||||||||||||||||||||||
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Neural cell adhesion molecule 1 (NCAM1), also called NCAM or CD56, is a protein that in humans is encoded by the NCAM1 gene (previously NCAM). It is a homophilic binding glycoprotein expressed on the surface of neurons, glia and skeletal muscle. Although CD56 is often considered a marker of neural lineage commitment due to its discovery site, CD56 expression is also found in, among others, the hematopoietic system. Here, the expression of CD56 is mostly associated with, but not limited to, natural killer cells. CD56 has been detected on other lymphoid cells, including gamma delta (γδ) Τ cells and activated CD8+ T cells, as well as on dendritic cells.[5] NCAM1 has been implicated as having a role in cell–cell adhesion,[6] neurite outgrowth, synaptic plasticity, and learning and memory.
NCAM1 is a glycoprotein of the Immunoglobulin (Ig) superfamily. At least 27 alternatively spliced NCAM1 mRNAs are produced, giving a wide diversity of NCAM1 isoforms.[7] The three main isoforms of NCAM1 vary only in their cytoplasmic domain:
The extracellular domain of NCAM1 consists of five immunoglobulin-like (Ig) domains followed by two fibronectin type III (FNIII) domains. The different domains of NCAM1 have been shown to have different roles, with the Ig domains being involved in homophilic binding to NCAM1, and the FNIII domains being involved signalling leading to neurite outgrowth.
Homophilic binding occurs between NCAM1 molecules on opposing surfaces (trans-) and NCAM1 molecules on the same surface (cis-)1. There is much controversy as to how exactly NCAM1 homophilic binding is arranged both in trans- and cis-. Current models suggest trans- homophilic binding occurs between two NCAM1 molecules binding antiparallel between all five Ig domains or just IgI and IgII. cis- homophilic binding is thought to occur by interactions between both IgI and IgII, and IgI and IgIII, forming a higher order NCAM1 multimer. Both cis- and trans- NCAM1 homophilic binding have been shown to be important in NCAM1 "activation" leading to neurite outgrowth.
Another layer of complexity is created by the insertion of other "minor" exons in the NCAM1 transcript. The two most notable are:
NCAM1 exhibits glycoforms as it can be posttranslationally modified by the addition of polysialic acid (PSA) to the fifth Ig domain, which is thought to abrogate its homophilic binding properties and can lead to reduced cell adhesion important in cell migration and invasion. PSA has been shown to be critical in learning and memory. Removal of PSA from NCAM1 by the enzyme endoneuraminidase (EndoN) has been shown to abolish long-term potentiation (LTP) and long-term depression (LTD).[9][10][11]
The neural cell adhesion molecule NCAM1 appears on early embryonic cells and is important in the formation of cell collectives and their boundaries at sites of morphogenesis.
Later in development, NCAM1 (CD56) expression is found on various differentiated tissues and is a major CAM mediating adhesion among neurons and between neurons and muscle.
NCAM1 is thought to signal to induce neurite outgrowth via the fibroblast growth factor receptor (FGFR) and act upon the p59Fyn signaling pathway.
In nerves, NCAM1 regulates homophilic (like-like) interactions between neurons and between neurons and muscle; it associates with fibroblast growth factor receptor (FGFR) and stimulates tyrosine kinase activity of receptor to induce neurite outgrowth. When neural crest cells stop making N-CAM and N-cadherin, and start displaying integrin receptors, cells separate and migrate.
During hematopoiesis, CD56 is the prototypic marker of NK cells, also present on subset of CD4+ T cells and CD8+ T cells.
In cell adhesion, CD56 contributes to cell-cell adhesion or cell-matrix adhesion during embryonic development.
In anatomic pathology, pathologists make use of CD56 immunohistochemistry to recognize certain tumors.
NCAM1 has been identified as one of the target proteins for both the rabies and zika virus, allowing entry into the cell.[12][13]
NCAM1 has been used as a target molecule for experimental antibody-based immunotherapy. Successful radio-immunolocalisation of metastases was demonstrated after giving injections of NCAM1-binding 123J-UJ13a or 131J-UJ13a radio-immunoconjugates to children with neuroblastoma. Patients with small cell lung cancer were treated with the anti-NCAM1 immunotoxin huN901-DM1 in two different clinical studies, revealing acceptable toxicity and signs of clinical response.[14]
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Source: Wikipedia. Article content is retrieved live through the MediaWiki API.
Neural cell adhesion molecule 1 (NCAM1), also called NCAM or CD56, is a protein that in humans is encoded by the NCAM1 gene (previously NCAM). It is a homophilic binding glycoprotein expressed on the surface of neurons, glia and skeletal muscle. Although CD56 is often considered a marker of neural lineage commitment due to its discovery site, CD56 expression is also found in, among others, the hematopoietic system. Here, the expression of CD56 is mostly associated with, but not limited to, natural killer cells. CD56 has been detected on other lymphoid cells, including gamma delta (γδ) Τ cells and activated CD8+ T cells, as well as on dendritic cells. NCAM1 has been implicated as having a role in cell–cell adhesion, neurite outgrowth, synaptic plasticity, and learning and memory.
CD5 is a cluster of differentiation expressed on the surface of T cells (various species) and in a subset of murine B cells known as B-1a. The expression of this receptor in human B cells has been a controversial topic and to date there is no consensus regarding the role of this receptor as a marker of human B cells. B-1 cells have limited diversity of their B-cell receptor due to their lack of the enzyme terminal deoxynucleotidyl transferase (TdT) and are potentially self-reactive. CD5 serves to mitigate activating signals from the BCR so that the B-1 cells can only be activated by very strong stimuli (such as bacterial antigen) and not by normal tissue antigen. CD5 was used as a T-cell marker until monoclonal antibodies against CD3 were developed. In humans, the gene is located on the long arm of chromosome 11. There is no confirmed ligand for CD5 but there is evidence that CD72, a C-type lectin, may be a ligand or that CD5 may be homophilic, binding CD5 on the surface of other cells. CD5 includes a scavenger receptor cysteine-rich protein domain. T cells express higher levels of CD5 than B cells. CD5 is upregulated on T cells upon strong activation. In the thymus, there is a correlation with CD5 expression and strength of the interaction of the T cell towards self-peptides.
Signaling lymphocytic activation molecule (SLAM) is a family of genes. Homophilic binding between SLAMs is involved in cell-to-cell adhesion during antigen presentation. Signaling lymphocytic activation molecules are a CD2-related surface receptor expressed by activated phagocytes, T helper cells, and platelets. SLAMs have a variety of functions, including enhancing T cellular proliferation by stimulating IL-4 and IFN-gamma production. SLAM family (SLAMF) receptors can interact directly with microbes, which can cause phagocytic cells to migrate to the area. SLAMF activation can trigger SLAM-associated protein (SAP) activation and a defective SAP can cause X-linked lymphoproliferative syndrome (XLP).
A desmosome (; "binding body"), also known as a macula adherens (plural: maculae adherentes) (Latin for adhering spot), is a cell structure specialized for cell-to-cell adhesion. A type of junctional complex, they are localized spot-like adhesions randomly arranged on the lateral sides of plasma membranes. Desmosomes are one of the stronger cell-to-cell adhesion types and are found in tissue that experience intense mechanical stress, such as cardiac muscle tissue, bladder tissue, gastrointestinal mucosa, and epithelia.
Before the 1921 destruction of Tulsa’s Greenwood District, Black residents had created a remarkable center of business and community life. The district included stores, professional offices, entertainment venues and homes owned by Black citizens. Understanding Greenwood means learning what was built—not only what was burned.
MORE →Madam C.J. Walker
