FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1497232715> ?p ?o ?g. }

• W1497232715 abstract "G protein-coupled receptor (GPCR) kinase (GRK)2 regulates the responsiveness of many GPCRS, e.g. CCR1, CCR2, CCR5, neurokinin-1 receptor, and metabotropic glutamate receptors, which are involved in the development of allodynia (pain due to a stimulus which does normally not provoke pain) and hyperalgesia (an increased response to a painful stimulus). During several inflammatory processes, the amount of cellular GRK2 is modulated in leukocytes, which has consequences for GPCR function. In general, a reduction in GRK2 expression correlates with enhanced receptor signaling, whereas an increase in GRK2 associates with decreased receptor function. In addition, the amount of cellular GRK2 determines the course and outcome of the disease. The experiments performed in this thesis focused on: 1. the expression of spinal cord neuronal GRK2 during neuropathic pain, 2. the consequences of low GRK2 on pain perception, 3. the mechanism of GRK2-mediated regulation of GPCR signaling. We demonstrated a reduction of neuronal GRK2 in the spinal cord dorsal horn during two models of nerve injury-induced mechanical allodynia: chronic constriction injury (CCI) of the sciatic nerve in rats and L5 spinal nerve transection (SNT) in mice. In addition, we reported that interleukin (IL)-1 type 1 receptor knock-out (IL-1R-/-) mice did not show a reduction in spinal cord GRK2 during L5 SNT and also did not develop mechanical allodynia in this model. Furthermore, chronic IL-1 1β treatment of ex vivo cultured spinal cord slices resulted in a decrease in GRK2. These data demonstrate a role for IL-1 1β signaling in downregulating spinal cord GRK2 during mechanical allodynia. Moreover, we showed that low GRK2 lead to increased mechanical allodynia and thermal hyperalgesia in animals with paw inflammation. No changes in pain perception were observed in naive GRK2+/- mice compared to wild type (WT) mice. Finally, we reported that GRK2 not only plays a role in neurons, but also in astrocytes by regulating GPCR (chemokine) signaling in primary cultures of astrocytes via interaction with intracellular signaling molecules. Further elucidation of the function of GRK2 during states of increased pain perception might uncover new opportunities for the treatment of patients with chronic pain." @default.
• W1497232715 created "2016-06-24" @default.
• W1497232715 creator A5064224386 @default.
• W1497232715 date "2007-12-11" @default.
• W1497232715 modified "2023-09-27" @default.
• W1497232715 title "GRK2 deficiency is a pain" @default.
• W1497232715 cites W141463146 @default.
• W1497232715 cites W1527988408 @default.
• W1497232715 cites W1533386139 @default.
• W1497232715 cites W1538620682 @default.
• W1497232715 cites W1550545417 @default.
• W1497232715 cites W1567615855 @default.
• W1497232715 cites W1588041244 @default.
• W1497232715 cites W1606957740 @default.
• W1497232715 cites W1818221350 @default.
• W1497232715 cites W1879507096 @default.
• W1497232715 cites W1919059205 @default.
• W1497232715 cites W1933410007 @default.
• W1497232715 cites W1942463334 @default.
• W1497232715 cites W1942930266 @default.
• W1497232715 cites W1964918370 @default.
• W1497232715 cites W1964953009 @default.
• W1497232715 cites W1965431554 @default.
• W1497232715 cites W1965866432 @default.
• W1497232715 cites W1967767166 @default.
• W1497232715 cites W1968322025 @default.
• W1497232715 cites W1968618759 @default.
• W1497232715 cites W1970548320 @default.
• W1497232715 cites W1974093633 @default.
• W1497232715 cites W1974241409 @default.
• W1497232715 cites W1974530349 @default.
• W1497232715 cites W1975096151 @default.
• W1497232715 cites W1975403276 @default.
• W1497232715 cites W1977033769 @default.
• W1497232715 cites W1979197099 @default.
• W1497232715 cites W1979359788 @default.
• W1497232715 cites W1979793055 @default.
• W1497232715 cites W1980674121 @default.
• W1497232715 cites W1981572127 @default.
• W1497232715 cites W1984025105 @default.
• W1497232715 cites W1985260340 @default.
• W1497232715 cites W1986809710 @default.
• W1497232715 cites W1987332793 @default.
• W1497232715 cites W1987704983 @default.
• W1497232715 cites W1989274659 @default.
• W1497232715 cites W1989707466 @default.
• W1497232715 cites W1991705906 @default.
• W1497232715 cites W1992206444 @default.
• W1497232715 cites W1994493683 @default.
• W1497232715 cites W1994816216 @default.
• W1497232715 cites W1995705528 @default.
• W1497232715 cites W1998185338 @default.
• W1497232715 cites W1999530386 @default.
• W1497232715 cites W2000814289 @default.
• W1497232715 cites W2001373534 @default.
• W1497232715 cites W2001809015 @default.
• W1497232715 cites W2003266871 @default.
• W1497232715 cites W2003646312 @default.
• W1497232715 cites W2004755236 @default.
• W1497232715 cites W2006161356 @default.
• W1497232715 cites W2006424917 @default.
• W1497232715 cites W2010629344 @default.
• W1497232715 cites W2011564897 @default.
• W1497232715 cites W2012387535 @default.
• W1497232715 cites W2012928472 @default.
• W1497232715 cites W2014007136 @default.
• W1497232715 cites W2015834221 @default.
• W1497232715 cites W2015893386 @default.
• W1497232715 cites W2016315302 @default.
• W1497232715 cites W2017047842 @default.
• W1497232715 cites W2017537032 @default.
• W1497232715 cites W2020518352 @default.
• W1497232715 cites W2020877995 @default.
• W1497232715 cites W2020919177 @default.
• W1497232715 cites W2022052400 @default.
• W1497232715 cites W2025030241 @default.
• W1497232715 cites W2025771548 @default.
• W1497232715 cites W2026325027 @default.
• W1497232715 cites W2026439530 @default.
• W1497232715 cites W2028125482 @default.
• W1497232715 cites W2029047992 @default.
• W1497232715 cites W2029052547 @default.
• W1497232715 cites W2032568216 @default.
• W1497232715 cites W2032848541 @default.
• W1497232715 cites W2034056966 @default.
• W1497232715 cites W2034949619 @default.
• W1497232715 cites W2035202152 @default.
• W1497232715 cites W2039193709 @default.
• W1497232715 cites W2039784545 @default.
• W1497232715 cites W2040372727 @default.
• W1497232715 cites W2043974564 @default.
• W1497232715 cites W2044188934 @default.
• W1497232715 cites W2045781877 @default.
• W1497232715 cites W2047025362 @default.
• W1497232715 cites W2047920258 @default.
• W1497232715 cites W2048415064 @default.
• W1497232715 cites W2049390031 @default.
• W1497232715 cites W2052750950 @default.
• W1497232715 cites W2055197670 @default.
• W1497232715 cites W2055910542 @default.

• next