Subunit-Specific Regulation of Kir3 Channels by Sorting nexin 27

Nassirpour, Rounak; Slesinger, Paul A.

doi:10.4161/chan.5191

Cited by 15 publications

(11 citation statements)

References 14 publications

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“…In contrast to SNX27b, expression of SNX27b-ΔRA did not significantly change I Baclofen (–55 pA/pF) with GIRK2c/3 channels ( Figure 1C, D ). Similarly, SNX27b-ΔRA did not significantly alter I Baclofen for HEK293T cells expressing GIRK1/3 channels ( Figure 1D ), in contrast to previous studies where wild-type SNX27b consistently reduced GIRK1/3 currents [7], [8], [23]. Thus, removal of the RA domain appeared to interfere with the ability of SNX27b to regulate GIRK3-containing channels in HEK293T cells.…”

Section: Resultscontrasting

confidence: 59%

Ras-Association Domain of Sorting Nexin 27 Is Critical for Regulating Expression of GIRK Potassium Channels

et al. 2013

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G protein-gated inwardly rectifying potassium (GIRK) channels play an important role in regulating neuronal excitability. Sorting nexin 27b (SNX27b), which reduces surface expression of GIRK channels through a PDZ domain interaction, contains a putative Ras-association (RA) domain with unknown function. Deleting the RA domain in SNX27b (SNX27b-ΔRA) prevents the down-regulation of GIRK2c/GIRK3 channels. Similarly, a point mutation (K305A) in the RA domain disrupts regulation of GIRK2c/GIRK3 channels and reduces H-Ras binding in vitro. Finally, the dominant-negative H-Ras (S17N) occludes the SNX27b-dependent decrease in surface expression of GIRK2c/GIRK3 channels. Thus, the presence of a functional RA domain and the interaction with Ras-like G proteins comprise a novel mechanism for modulating SNX27b control of GIRK channel surface expression and cellular excitability.

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Section: Resultscontrasting

confidence: 59%

Ras-Association Domain of Sorting Nexin 27 Is Critical for Regulating Expression of GIRK Potassium Channels

et al. 2013

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“…The second gene, hTax1 (human T-cell leukemia virus type I) binding protein 1 ( hTax1BP1 ), encodes a cytoplasmic protein that inhibits TNF-induced apoptosis by mediating the anti-apoptotic activity of TNFAIP3 and that may also have a role in the pro-inflammatory cytokine IL-1 signaling cascade [95]. The third gene, human sorting nexin family member 27 ( hSNX27 ), encodes a cytoplasmic protein that is involved in cellular endocytic trafficking and the T lymphocyte endocytic recycling pathway [96]. The last gene, human cyclin A2 ( hCycA2 ), encodes a protein belonging to the highly conserved cyclin family, which is a key component of the cell cycle machinery, and functions as a regulator of cyclin-dependent kinases [97].…”

Section: Resultsmentioning

confidence: 99%

Methanol May Function as a Cross-Kingdom Signal

et al. 2012

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Recently, we demonstrated that leaf wounding results in the synthesis of pectin methylesterase (PME), which causes the plant to release methanol into the air. Methanol emitted by a wounded plant increases the accumulation of methanol-inducible gene mRNA and enhances antibacterial resistance as well as cell-to-cell communication, which facilitates virus spreading in neighboring plants. We concluded that methanol is a signaling molecule involved in within-plant and plant-to-plant communication. Methanol is considered to be a poison in humans because of the alcohol dehydrogenase (ADH)-mediated conversion of methanol into toxic formaldehyde. However, recent data showed that methanol is a natural compound in normal, healthy humans. These data call into question whether human methanol is a metabolic waste product or whether methanol has specific function in humans.Here, to reveal human methanol-responsive genes (MRGs), we used suppression subtractive hybridization cDNA libraries of HeLa cells lacking ADH and exposed to methanol. This design allowed us to exclude genes involved in formaldehyde and formic acid detoxification from our analysis. We identified MRGs and revealed a correlation between increases in methanol content in the plasma and changes in human leukocyte MRG mRNA levels after fresh salad consumption by volunteers. Subsequently, we showed that the methanol generated by the pectin/PME complex in the gastrointestinal tract of mice induces the up- and downregulation of brain MRG mRNA. We used an adapted Y-maze to measure the locomotor behavior of the mice while breathing wounded plant vapors in two-choice assays. We showed that mice prefer the odor of methanol to other plant volatiles and that methanol changed MRG mRNA accumulation in the mouse brain.We hypothesize that the methanol emitted by wounded plants may have a role in plant-animal signaling. The known positive effect of plant food intake on human health suggests a role for physiological methanol in human gene regulation.

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“…These results are consistent with the possible role of GIRK3 as a negative regulator of GIRK channel surface trafficking. In midbrain DA neurons, GIRK3 mediates an interaction between the GIRK channel, a GIRK2c/GIRK3 heteromer 13 , and SNX-27 36, 50, 51 , a protein implicated in the surface trafficking and internalization of several channels and receptors 52–56 . The interaction between SNX-27 and GIRK3 is conferred by a Class I PDZ interaction domain at the GIRK3 C-terminus, which is identical to that found in GIRK2c 33 .…”

Section: Discussionmentioning

confidence: 99%

GIRK2 splice variants and neuronal G protein-gated K+ channels: implications for channel function and behavior

Velasco

Zhang

et al. 2017

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Many neurotransmitters directly inhibit neurons by activating G protein-gated inwardly rectifying K+ (GIRK) channels, thereby moderating the influence of excitatory input on neuronal excitability. While most neuronal GIRK channels are formed by GIRK1 and GIRK2 subunits, distinct GIRK2 isoforms generated by alternative splicing have been identified. Here, we compared the trafficking and function of two isoforms (GIRK2a and GIRK2c) expressed individually in hippocampal pyramidal neurons lacking GIRK2. GIRK2a and GIRK2c supported comparable somato-dendritic GIRK currents in Girk2 −/− pyramidal neurons, although GIRK2c achieved a more uniform subcellular distribution in pyramidal neurons and supported inhibitory postsynaptic currents in distal dendrites better than GIRK2a. While over-expression of either isoform in dorsal CA1 pyramidal neurons restored contextual fear learning in a conditional Girk2 −/− mouse line, GIRK2a also enhanced cue fear learning. Collectively, these data indicate that GIRK2 isoform balance within a neuron can impact the processing of afferent inhibitory input and associated behavior.

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Subunit-Specific Regulation of Kir3 Channels by Sorting nexin 27

Cited by 15 publications

References 14 publications

Ras-Association Domain of Sorting Nexin 27 Is Critical for Regulating Expression of GIRK Potassium Channels

Ras-Association Domain of Sorting Nexin 27 Is Critical for Regulating Expression of GIRK Potassium Channels

Methanol May Function as a Cross-Kingdom Signal

GIRK2 splice variants and neuronal G protein-gated K+ channels: implications for channel function and behavior

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