Aperçu des produits pour anti-GNAT1 (GNAT1) Anticorps

Cow (Bovine) Guanine Nucleotide Binding Protein (G Protein), alpha Transducing Activity Polypeptide 1 (GNAT1) interaction partners

1. Data suggest that a hetero-multimer complex forms between light-activated rhodopsin and light-activated heterotrimeric transducin (T-alpha-1, Gnb1, Gngt1); the stoichiometry is 1:1 rhodopsin:transducin. The complex appears to form on native rod outer segment membranes upon light activation.

2. These results indicated that efficient Gt activation by rhodopsin, resulting from an optimized active state of rhodopsin, is one of the causes of the high amplification efficiency of rods.

Human Guanine Nucleotide Binding Protein (G Protein), alpha Transducing Activity Polypeptide 1 (GNAT1) interaction partners

1. Our family's ERG showed essentially no rod response, consistent with a Danish GNAT1 pedigree but different from the Nougaret GNAT1 pedigree that shows partial preservation of rod signal. A genetic connection between Complete congenital stationary night blindness and postural orthostatic tachycardia syndrome would be intriguing, but we found no evidence for this.

2. These data suggest that some truncating GNAT1 variants can indeed cause a recessive, mild, late-onset retinal degeneration in human beings rather than just stationary night-blindness as reported previously.

3. Three candidate tumor-suppressor genes, SEMA3B, AXUD1 and GNAT1 may be involved in oral squamous cell carcinoma.

4. These data suggest that a homozygous missense mutation in GNAT1 is associated with autosomal recessive stationary night blindness.

5. Expression of GNAT1 gene is down-regulated or absent in nasopharyngeal carcinoma tissues.

Mouse (Murine) Guanine Nucleotide Binding Protein (G Protein), alpha Transducing Activity Polypeptide 1 (GNAT1) interaction partners

1. In conclusion, deletion of transducin1 (and the resulting inhibition of phototransduction in rod cells) inhibits the development of retinal vascular pathology in early diabetic retinopathy.

2. we generated double-mutant (Pde6c(cpfl1/cpfl1)Gnat1(IRD2/IRD2)) mice with absent rod and cone photoreceptor function, and we evaluated their response for restoring rod (GNAT1) function through gene therapy

3. an estimate for the electrical effect from a single transducin-cGMP-phosphodiesterase catalytic subunit molecular complex in intact mouse rods., is reported

4. GNAT1 role in phototransduction of rod photoreceptors

5. Data suggest light reduces oxygen consumption rate (OCR) of retina; light does not affect OCR in retinas of Gnat1-/- knockout mice (phototransduction disabled). Light reduces cGMP in retina; light does not alter cGMP in Gnat1-/- plus Gnat2-/- retina.

6. Biochemical changes, including reduced transducin protein levels and enhanced transducin GTPase activity, explain the shift in light intensity threshold for Galphat1 translocation in Rs1-knockout mice.

7. The results from shaker1 and whirler mice suggest that defective transducin translocation may be functionally related to light-induced degeneration.

8. ectopically expressed cTalpha 1) forms a heterotrimeric complex with rod Gbeta(1)gamma(1), and substitutes equally for rTalpha in generating photoresponses initiated by either rhodopsin or S-cone opsin

9. Oligomerization incompetent retinal degeneration slow is associated with mislocalization of cone opsins and cone transducin.

10. Data show that visual responses in TKO mice extend beyond the retina to encompass the lateral margins of the lateral geniculate nucleus and components of the visual cortex.

11. Thus our results showed that IRD1 and IRD2 mice harbor a nonsense mutation in the Gnat1 gene, resulting in the absence or suppressed expression of the Tralpha protein, which is the likely cause of rod dysfunction in both mutants.

12. alpha-transducin can function in taste receptor cells and transduce some taste cell responses

13. data suggest that phosducin action is based on the reduction of transducin affinity to the membranes of rod outer segments, achieved by keeping the transducin beta gamma subunits apart from the alpha subunit.

14. Alpha-transducin played no role in regulating adaptive response to light. Degeneration does not require transducin-mediated signaling.

15. Alpha-transducin played no role in responses to salty, bitter, & sweet compounds or to inosine monophoshate. It was involved in the umami taste of MSG & monopotassium glutamate. Umami detection by alpha-transducin occurs in anteriorly placed taste buds.

16. The localization and interaction with Gtalpha suggest LGN roles in modulation of transducin translocation and other photoreceptor cell functions.

17. the light-dependent translocations of transducin are controlled by the GTP-hydrolysis on Gtalpha, and apparently, do not require Gtalpha interaction with RGS9 and PDE6

18. alpha transducin and opsin have roles in mouse photoreceptor cell responses to light and dark

19. The light-dependency threshold for transducin translocation is determined by the balance between the rate of transducin dissociation from membranes and the capacity of the GTPase-activating complex.

20. Phosducin does not contribute to adaptation mechanisms of the outer segment by dynamically controlling heterotrimer availability, but is necessary for maintaining normal transducin expression and therefore normal flash sensitivity in rods.