D- and l-Amphetamine differentially mediates self-stimulation in rat dorsal midbrain area

Ellman, Steven J.; Ackermann, Robert F.; Bodnar, Richard J.; Jackler, Frances; Steiner, Solomon S.

doi:10.1016/0031-9384(76)90184-0

Cited by 11 publications

(3 citation statements)

References 32 publications

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“…These neutrophils appeared to produce lower levels of pro-inflammatory cytokines, but higher levels of IL-22 and transforming growth factor-b and higher bactericidal actives. CD177-positive neutrophils appear to play a protective role in inflammatory bowel disease by increasing bactericidal activity and IL-22 [65].…”

Section: Functions Of Cd177mentioning

confidence: 99%

“…Over production of red blood cells, increased platelet and neutrophil counts and splenomegaly are the predominant characteristics of this disease [33]. Studies on polycythemia vera revealed that 95-100% of patients have elevated levels of CD177 mRNA [33,[65][66][67][68][69][70]. CD177 appears to be the only gene strongly overexpressed in these patients [33].…”

Section: Cd177 In Diseasementioning

confidence: 99%

“…CD177 appears to be the only gene strongly overexpressed in these patients [33]. Besides overexpression of CD177 in polycythemia vera patients, it appears that CD177 is also overexpressed in other myeloproliferative disorders including essential thrombocythemia and idiopathic myelofibrosis [33,[65][66][67][68][69][70]. Overall, neutrophil CD177 expression is found to be increased in 65 -97% of polycythemia vera patients, in 32 -57% of essential thrombocythemia patients, and in 43 -50% of idiopathic myelofibrosis patients [33,[71][72][73].…”

Section: Cd177 In Diseasementioning

confidence: 99%

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The multifaceted roles of CD177 in mammary tissue development and breast cancer

Kluz¹

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Aiming to identify immune molecules with a novel function in cancer pathogenesis, we found the cluster of differentiation 177 (CD177), a known neutrophil antigen, expression to be positively correlated with relapse-free (RFS), metastasis-free (MFS) or overall survival (OS) in several solid cancers including those from breast, prostate, cervix, and lung. To study the role of CD177 in breast cancer, we generated a total body Cd177 knockout mouse. These mice had no profound phenotype at 3-months of age or younger. The only phenotype found at this age was reduced peripheral neutrophil counts, but no difference in their ability to clear infections. Upon further analysis these mice developed an age dependent hyperproliferative mammary gland phenotype at 10-months of age that was lost in mice 15-months and older. Focusing on breast cancer, we found that CD177 is expressed in normal breast epithelial cells and is significantly reduced in invasive cancer. We found that CD177 suppresses breast cancer pathogenesis. To understand the mechanism behind CD177 mediated suppression of breast cancer, we performed mass spectrometry on the purified CD177 complex. Mass spectrometry and co-immunoprecipitation results revealed CD177 interacts with b-Catenin and glycolytic enzymes PFK, aldolase A, GAPDH and enolasea. Further studies revealed that mechanistically CD177 forms a complex with E-Cadherin and b-Catenin at adherens junctions. This physical interaction between CD177, E-Cadherin and b-Catenin prevents b-Catenin activation via the canonical WNT. We also found CD177 suppressed WNT/b-Catenin signaling independent of E-Cadherin with an unknown protein. Thus, we identified a novel protein complex involving CD177 and proteins from adherens junctions that can suppress cancer formation via inhibiting the v WNT/b-Catenin signaling pathway, a key cellular biological process relevant to the oncogenesis of multiple cancer types and tissue development. The lack of WNT/b-Catenin signaling control explains how mice without CD177 develop hyperproliferation of mammary epithelium in the mouse mammary gland. Interestingly, this phenotype is lost with age, possibly due to a decrease in WNT/b-Catenin signaling resulting from a decrease in progesterone and estrogen. In addition to CD177's role in the regulation of WNT/b-Catenin signaling we also identified that CD177 plays a role in cancer cell metabolism. Since metabolism plays a significant role in cancer and CD177 interacts with glycolytic enzymes, we sought to determine if CD177 plays a role in metabolism. CD177 appears to interact with glycolytic enzymes, PFK, aldolase A, GAPDH, and a-enolase and ultimately suppresses their mRNA expression. Furthermore, we found novel localization of CD177 at the mitochondrion, thus providing a potential explanation as to how an extracellular membrane bound protein such as CD177 interacts with glycolytic enzymes. Metabolic analysis of CD177 expression on cancer cells revealed that CD177 leads to a decrease in glucose uptake and a slight decrease in basal glycoly...

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Section: Functions Of Cd177mentioning

confidence: 99%