Disease relevance of JMJD6

• Elastase-mediated phosphatidylserine receptor cleavage impairs apoptotic cell clearance in cystic fibrosis and bronchiectasis [1].
• Therefore, defective airway clearance of apoptotic cells in cystic fibrosis and bronchiectasis may be due to elastase-mediated cleavage of phosphatidylserine receptor on phagocytes and may contribute to ongoing airway inflammation [1].
• Phosphatidylserine receptor in chronic pancreatitis: evidence for a macrophage independent role [2].
• A specific receptor for phosphatidylserine (PSR) has recently been identified by phage display and shown to mediate phosphatidylserine dependent phagocytosis [3].
• CONCLUSION: L-[1-C-11]-tyrosine is a valid tracer for diagnosis of brain tumors and allowed quantification of PSR [4].

Psychiatry related information on JMJD6

• At follow-up, patients participated in a 4 to 6 hour interview that assessed current and lifetime Axis I disorders (SCID-I), current Axis II disorders (PDE), eating behaviors (EAT, BSQ, EDI, PSR), global functioning (GAF), social adjustment (SAS-SR), and treatment and medical problems experienced since discharge [5].
• This paper reports on turnover intentions of PSR workers, a rapidly growing sector of the community mental health labor force as reported in a nationwide survey [6].
• The present study examined the relationship between the perception by homosexual males of positive or negative societal reaction to homosexuality (PSR), their degree of conformity to heterosexual norms, and their degree of psychological adjustment [7].

High impact information on JMJD6

• This candidate phosphatidylserine receptor is highly homologous to genes of unknown function in Caenorhabditis elegans and Drosophila melanogaster, suggesting that phosphatidylserine recognition on apoptotic cells during their removal by phagocytes is highly conserved throughout phylogeny [8].
• Phagocytes interact with PS on apoptotic cells through either the PS receptor or secreted bridging proteins called opsonins [9].
• Resolution of inflammation is normally associated with the orderly removal of dying apoptotic inflammatory cells through cell recognition receptors, such as the phosphatidylserine receptor, CD36, and alpha v integrins [1].
• Cleavage of the phosphatidylserine receptor by neutrophil elastase specifically disrupted phagocytosis of apoptotic cells, implying a potential mechanism for delayed apoptotic cell clearance in vivo [1].
• Phosphatidylserine (PS) induces PS receptor-mediated macropinocytosis and promotes clearance of apoptotic cells [10].

Chemical compound and disease context of JMJD6

• Combinations of inhibitory and subinhibitory concentrations of thienamycin with 55 vol% of defibrinated human blood resulted in additive effects against all PSR and NSS test strains of S. marcescens and against the NSS Escherichia coli control strain ATCC 25922 [11].
• Although hypoxia (fractional concentration of O2 in air = 0.06) had no significant effect on fictive breathing, ventilating frogs with increasing CO2 levels (fractional CO2 concentration in inspired air range: 0.00-0.03) increased the number of breaths in each fictive breathing episode, and this effect was potentiated by PSR feedback [12].
• We concluded: (i) [15N]glycine cannot be used to measure the PSR in patients with evidence of liver disease; the results are best interpreted in terms of glycine metabolism; (ii) the "apparent" PSR correlated with clinical status; and (iii) an elevated PSR in a patient with a malignancy is not necessarily due to protein metabolism by the tumor [13].

Biological context of JMJD6

• Recently, a putative phosphatidylserine receptor (PSR) was identified and proposed to mediate recognition of phosphatidylserine and phagocytosis [14].
• Apoptosis was detected by the TUNEL method, and the RNA protection assay (RPA) was used to compare activation of apoptosis with PSR mRNA expression levels [2].
• Up-regulation of PSR could be confirmed by Western blot analysis [2].
• The RNA protection assay revealed high mRNA levels of the antiapoptotic genes bcl-2 and bfl-1 (P < 0.05) in chronic pancreatitis tissues with high PSR mRNA expression [2].
• Genetic deficiency of PSR in the mouse is lethal perinatally, and results to date have been ambiguous with regard to the phagocytic and inflammatory phenotypes associated with that deficiency [15].

Anatomical context of JMJD6

• These results allowed us to conclude that SR-BI is a phagocytosis-inducing PS receptor of Sertoli cells [16].
• The phosphatidylserine receptor is expressed on the surface of macrophages and is crucial for the recognition and engulfment of apoptotic cells [2].
• A newly described phosphatidylserine receptor, critical in the phagocytosis of apoptotic cells by macrophages, is also expressed at similar levels on human microglia [17].
• Our results suggest that both PSR and SR-B1 are expressed in nursing TECs and these receptors appear to play a major role in the clearance of apoptotic cells from the thymus [18].
• We conclude that PET can be used to estimate skeletal muscle PSR in healthy human subjects and that it holds promise for future in vivo, noninvasive studies of the influences of physiological factors, pharmacological manipulations, and disease states on this important component of muscle protein turnover and balance [19].

Associations of JMJD6 with chemical compounds

• PSR was calculated from fitted parameter values and plasma methionine concentrations [20].
• Engulfment of apoptotic eosinophils by A549 cells involved alpha(v)beta3-, CD36-, alpha(v)beta5-, and phosphatidylserine receptor-mediated recognition mechanisms and was associated with the formation of integrin focal adhesion complexes around apoptotic eosinophils [21].
• METHODS: A549 epithelial-cell expression of alpha(v)beta3, alpha(v)beta5, CD36, and the phosphatidylserine receptor was established by using immunostaining and flow cytometry, and inhibition assays were examined by using the role of these receptors in apoptotic-eosinophil recognition by resting and dexamethasone-treated A549 epithelial cells [21].
• The polyserine tract within the phosphatidylserine receptor protein is used as an excellent example of one such case [22].
• The increased phagocytosis of apoptotic neutrophils by ERY was also found to be phosphatidylserine receptor-dependent for AM [23].

Other interactions of JMJD6

• Here we demonstrate that CD14 does not function preferentially as a PS receptor in apoptotic-cell clearance [24].
• Different populations of macrophages use either the vitronectin receptor or the phosphatidylserine receptor to recognize and remove apoptotic cells [25].

Analytical, diagnostic and therapeutic context of JMJD6

• METHODS: The expression and localization of PSR were analyzed by Northern blot analysis, RT-PCR, Western blot analysis and immunohistochemistry [2].
• Indeed, affinity-purified anti-PSR antibodies identified a 47 kDa protein species in cells transfected with untagged PSR and localized this protein in the nuclei by immunofluorescent confocal microscopy [3].
• Ligation of PSR by PS on AC surfaces is considered essential for signaling uptake of ACs that are tethered to phagocytes via other receptors [26].
• Positron emission tomography (PET) with L-[methyl-11C]methionine was explored as an in vivo, noninvasive, quantitative method for measuring the protein synthesis rate (PSR) in paraspinal and hind limb muscles of anesthetized dogs [20].
• For quantification of the protein synthesis rate (PSR), arterial cannulation with repeated blood sampling to obtain the plasma input function and a dynamic TYR PET study to calculate a time-activity curve are necessary [27].

References