Disease relevance of Ptprf

• DSCG significantly attenuated both IAR and LAR, and significantly inhibited the increase in intraluminal mucus during LAR, but had no effect on eosinophilia in BALF [1].
• In the guinea-pig model for bronchial asthma, biphasic increases in airway resistance (immediate asthmatic response, IAR, and late asthmatic response, LAR), as well as accumulated inflammatory cells in BALF, were observed after repeated antigen challenge [2].

Psychiatry related information on Ptprf

• Whereas LAR mice displayed greater acute morphine dependence than HAR mice, HA and LA mice did not differ [3].

High impact information on Ptprf

• Here, Tina Dalianis and Lars Ahrlund-Richter propose that one component of the F1 antiparent response results from competition between the two sets of parentally derived major histocompatibility complex (MHC) molecules for 'promiscuous' peptides [4].
• Analysis of homozygous mice carrying insertions in LAR and PTP kappa showed that both genes were effectively disrupted, but neither was essential for normal embryonic development [5].
• Transgenic mice deficient in the LAR protein-tyrosine phosphatase exhibit profound defects in glucose homeostasis [6].
• Overall, these data provide further evidence for an important role for LAR in the regulation of insulin action and glucose homeostasis in intact animals [6].
• LAR, a transmembrane PTPase expressed in insulin-sensitive tissues, acts as a negative regulator of insulin signaling in intact cell models [6].

Biological context of Ptprf

• Developmental expression of the cell adhesion molecule-like protein tyrosine phosphatases LAR, RPTPdelta and RPTPsigma in the mouse [7].
• The physiological role of LAR was studied in mice in which LAR expression was eradicated by insertional mutagenesis [6].
• In wild-type mice, LAR expression is regulated during pregnancy reaching maximum levels around Day 16 of gestation [8].
• This architecture suggests that LAR may function in cellular signalling by the regulation of tyrosine phosphorylation through cell-cell or cell-matrix interactions [8].
• During differentiation of PAX-5-deficient pre-BI cell line into non-T cell lineages, expression of LAR is switched off, but it is up-regulated during differentiation into thymocytes [9].

Anatomical context of Ptprf

• We found that LAR is expressed in basal lamina-associated epithelial tissues of (neuro)ectodermal, neural crest/ectomesenchyme and endodermal origin [7].
• Mammary glands of LAR-/- females were incapable of delivering milk due to an impaired terminal differentiation of alveoli at late pregnancy [8].
• We used gene targeting in mouse embryonic stem cells to generate mice lacking sequences encoding both LAR phosphatase domains [8].
• Thus, within the hemopoietic system, LAR appears to be a T cell lineage-specific receptor-type phosphatase [9].
• In contrast to the c-kit(+)B220(+)CD19(+) pre-BI cells from normal mice, counterparts of pre-BI cells from PAX-5-deficient mice express LAR, indicating that PAX-5-mediated commitment to the B cell lineage results in suppression of LAR [9].

Associations of Ptprf with chemical compounds

• 1. The effects of a mouse (IgG1 fraction) anti-CD 18 neutralizing antibody (R15.7) on allergen-induced late airway response (LAR), airway hyperresponsiveness (AHR) and cellular recruitment were investigated in an allergic rabbit model [10].
• Strikingly, in HA/LA and HAR/LAR mice, we find that an inverse relationship exists with respect to morphine antinociceptive sensitivity in the hot-plate and acetic acid abdominal constriction tests, respectively [11].
• BACKGROUND: Disodium cromoglycate (DSCG) is known to inhibit both immediate and late asthmatic responses (IAR and LAR) [1].
• HAR and LAR mice, selectively bred for high and low levorphanol analgesia, respectively, display equally large differences in their analgesic sensitivity to DAMGO, modest differences in sensitivity to DPDPE, and no differences in sensitivity to DELT [12].
• Finally, (S,S)-formoterol enhanced the inflammatory changes in the peribronchial and perivascular areas without affecting EAR, LAR or AHR, whereas (R,R)-formoterol reduced EAR, LAR and AHR as well as cellular infiltration in the lung tissue of these mice [13].

Other interactions of Ptprf

• These observations suggest that LAR enhances retinal ganglion cell neurite initiation whilst suppressing retinal ganglion cell survival, and that PTP-BL facilitates both retinal ganglion cell neurite initiation and survival of activated retinal glia [14].
• The LAR receptor-like protein tyrosine phosphatase is composed of two intracellular tyrosine phosphatase domains and a cell adhesion molecule-like extracellular region containing three immunoglubulin-like domains in combination with eight fibronectin type-III-like repeats [8].

Analytical, diagnostic and therapeutic context of Ptprf

• Using RNA in situ hybridization we compared the expression patterns of the cell adhesion molecule-like receptor-type protein tyrosine phosphatases LAR, RPTP sigma and RPTP sigma during mouse development [7].
• In euglycemic clamp studies, the LAR (-/-) mice exhibited a significant resistance to insulin-stimulated glucose disposal and suppression of hepatic glucose output [6].
• However, the magnitude of the LAR following treatment with R15.7 was significantly reduced when compared to LAR demonstrated on 1st challenge (P < 0.001) or to that of the control group on both challenges (P < 0.01) [10].
• Acute morphine dependence was compared in mice selectively-bred for high (HA) and low (LA) swim stress-induced analgesia and high (HAR) and low (LAR) levorphanol analgesia by counting the number of naloxone-precipitated jumps [3].
• Sequences encoding three "receptor-like" transmembrane PTPases were identified and two of these (known as LAR and LRP) were confirmed to be expressed in muscle by subsequent cDNA library screening and Northern blot analysis [15].

References