MOUSE ANTI RAT CD47 Azide Free

Price:
899 EUR
1078 USD
746 GBP
known as: MOUSE ANTI RAT CD47 Azide Free
Catalog number: genta-ABS0277
Product Quantity: 1 mg
Category:
Supplier: AbD

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Gene target: cd47

Related genes to: MOUSE ANTI RAT CD47 Azide Free

Symbol : cd47 NIH gene
chromosome : LG3
description : CD47 molecule
type of gene : protein-coding
Modification date : 2016-05-26

Related Pathways to: MOUSE ANTI RAT CD47 Azide Free

Gene about :Cd47
Pathway :Rn Spinal Cord Injury
Cd47

Related product to: MOUSE ANTI RAT CD47 Azide Free

Related Articles about: MOUSE ANTI RAT CD47 Azide Free

CD47 overexpression is associated with decreased neutrophil apoptosis/phagocytosis and poor prognosis in non-small-cell lung cancer patients.

Non-small-cell lung cancer (NSCLC) patients often exhibit neutrophilia, which has been associated with poor clinical outcomes. However, the mechanisms that lead to neutrophilia have not been fully established. CD47 is an antiphagocytic molecule that promotes neutrophil recruitment. - Source :PubMed

BRAF/MEK inhibitors promote CD47 expression that is reversible by ERK inhibition in melanoma.

The expression of CD47 on the cancer cell surface transmits "don't eat me" signalling that not only inhibits phagocytosis of cancer cells by phagocytes but also impairs anti-cancer T cell responses. Here we report that oncogenic activation of ERK plays an important role in transcriptional activation of CD47 through nuclear respiratory factor 1 (NRF-1) in melanoma cells. Treatment with BRAF/MEK inhibitors upregulated CD47 in cultured melanoma cells and fresh melanoma isolates. Similarly, melanoma cells selected for resistance to the BRAF inhibitor vemurafenib expressed higher levels of CD47. The increase in CD47 expression was mediated by ERK signalling, as it was associated with rebound activation of ERK and co-knockdown of ERK1/2 by siRNA diminished upregulation of CD47 in melanoma cells after exposure to BRAF/MEK inhibitors. Furthermore, ERK1/2 knockdown also reduced the constitutive expression of CD47 in melanoma cells. We identified a DNA fragment that was enriched with the consensus binding sites for NRF-1 and was transcriptionally responsive to BRAF/MEK inhibitor treatment. Knockdown of NRF-1 inhibited the increase in CD47, indicating that NRF-1 has a critical role in transcriptional activation of CD47 by ERK signalling. Functional studies showed that melanoma cells resistant to vemurafenib were more susceptible to macrophage phagocytosis when CD47 was blocked. So these results suggest that NRF-1-mediated regulation of CD47 expression is a novel mechanism by which ERK signalling promotes the pathogenesis of melanoma, and that the combination of CD47 blockade and BRAF/MEK inhibitors may be a useful approach for improving their therapeutic efficacy. - Source :PubMed

[CD47 receptor as a primary target for cancer therapy].

Recently, a number of new highly efficient antibody-based anticancer therapeutics have emerged. These receptor-binding antibodies have beneficial toxicity profiles associated with relatively mild side effects. Therefore, the search for novel surface proteins that are present on cancer cells and play important metabolic or defensive roles has intensified. Additionally, the therapeutic stimulation of patient's immune system in order to aim its components, specifically, phagocytes and cytotoxic T-lymphocytes, at tumor cells is gaining traction. This review is focused on the CD47 surface receptor, a ubiquitously expressed molecule, which could nevertheless serve as a therapeutic target due to its ability to simultaneously stimulate both natural and adaptive immune response. - Source :PubMed

CD47 surface stability is sensitive to actin disruption prior to inclusion within the band 3 macrocomplex.

CD47 is an important 'marker of self' protein with multiple isoforms produced though alternative splicing that exhibit tissue-specific expression. Mature erythrocytes express CD47 isoform 2 only, with membrane stability of this version dependent on inclusion within the band 3 macrocomplex, via protein 4.2. At present a paucity of information exists regarding the associations and trafficking of the CD47 isoforms during erythropoiesis. We show that CD47 isoform 2 is the predominant version maintained at the surface of expanding and terminally differentiating erythroblasts. CD47 isoforms 3 and 4 are expressed in all cell types tested except mature erythrocytes, but do not reach the plasma membrane in erythroblasts and are degraded by the orthochromatic stage of differentiation. To identify putative CD47 interactants, immunoprecipitation combined with Nano LC-MS/MS mass spectrometry was conducted on the erythroleukaemic K562 cell line, expanding and terminally differentiating primary erythroblasts and mature erythrocytes. Results indicate that prior to incorporation into the band 3 macrocomplex, CD47 associates with actin-binding proteins and we confirm that CD47 membrane stability is sensitive to actin disrupting drugs. Maintenance of CD47 at the cell surface was also influenced by dynamin, with sensitivity to dynamin disruption prolonged relative to that of actin during erythropoiesis. - Source :PubMed

Engineering macrophages to eat cancer: from "marker of self" CD47 and phagocytosis to differentiation.

The ability of a macrophage to engulf and break down invading cells and other targets provides a first line of immune defense in nearly all tissues. This defining ability to "phagos" or devour can subsequently activate the entire immune system against foreign and diseased cells, and progress is now being made on a decades-old idea of directing macrophages to phagocytose specific targets, such as cancer cells. Engineered T cells provide precedence with recent clinical successes against liquid tumors, but solid tumors remain a challenge, and a handful of clinical trials seek to exploit the abundance of tumor-associated macrophages instead. Although macrophage differentiation into such phenotypes with deficiencies in phagocytic ability can raise challenges, newly recognized features of cancer cells that might be manipulated to increase the phagocytosis of those cells include ≥1 membrane protein, CD47, which broadly inhibits phagocytosis and is abundantly expressed on all healthy cells. Physical properties of the target also influence phagocytosis and again relate-via cytoskeleton forces-to differentiation pathways in solid tumors. Such pathways extend to mechanosensing by the nuclear lamina, which is known to influence signaling by soluble retinoids that can regulate the macrophage SIRPα, the receptor for CD47. Here, we highlight some of those past, present, and rapidly emerging efforts to understand and control macrophages for cancer therapy. - Source :PubMed

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