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anti-Human PDE6B Antibodies:
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Cow (Bovine) Polyclonal PDE6B Primary Antibody for ICC, IF - ABIN267359
Dong, Claffey, Brocke, Epstein: Expression of phosphodiesterase 6 (PDE6) in human breast cancer cells. in SpringerPlus 2014
Cow (Bovine) Polyclonal PDE6B Primary Antibody for CM, ICC - ABIN2747182
Nikolova, Guenther, Savai, Weissmann, Ghofrani, Konigshoff, Eickelberg, Klepetko, Voswinckel, Seeger, Grimminger, Schermuly, Pullamsetti: Phosphodiesterase 6 subunits are expressed and altered in idiopathic pulmonary fibrosis. in Respiratory research 2011
Mutation in PDE6B gene is associated with autosomal recessive retinitis pigmentosa disease progression.
A novel PDE6B founder variant is likely to account for 16% of recessive inherited retinal dystrophy in Maori. Careful characterization of the clinical presentation permits identification of further Maori patients with a similar phenotype and simplifies the diagnostic algorithm.
Heterozygous mutation in the PDE6B gene can cause a reduction in the rod function to different degrees.
Next-generation whole exome sequencing revealed a homozygous c.1923_1969ins6del47 nonsense PDE6B mutation, which has not been previously described, that segregated with the disease in the family.
The family was found to segregate novel mutations of two different genes: myosin VIIA (MYO7A), and phosphodiesterase 6B, which causes nonsyndromic retinitis pigmentosa.
analysis of amino acid residues responsible for the selectivity of tadalafil binding to two closely related phosphodiesterases, PDE5 and PDE6
The p.H557Y mutation in PDE6B, was homozygous in four patients and heterozygous in nine patients, and it was the most frequent mutation (2.5%) in Korean patients with retinitis pigmentosa.
Data indicate the upregulation of RREB1, PDE6B, and CD209 suggests that these proteins might play important roles in the differentiation of primitive gut tube cells from embryonic stem cells (hESCs) and in primitive gut tube development into pancreas.
Mutations have been identified in the beta-subunit of rod phosphodiesterase in consanguineous Pakistani families with autosomal recessive retinitis pigmentosa.
Rod phosphodiesterase-6 PDE6A and PDE6B subunits are enzymatically equivalent.
Sp4 is a strong activator of transcription from the beta-PDE promoter
the rod cGMP-phosphodiesterase beta-subunit gene is transcriptionally and post-transcriptionally regulated [review]
Clinical and genetic characterization of a Chinese family with PDE6B is reported.
PDE6B genes and the phenotypic heterogeneity and particularly the severe ocular affection first observed in one Usher syndrome patient.
These studies indicate that the 3' UTR of the PDEbeta mRNA is involved in the complex regulation of this gene's expression in the retina.
The approximately 11 A map revealed previously unseen features of PDE6, and each domain was readily fit with high resolution structures.
Structural analysis of cGMP phosphodiesterase 6 alpha, beta and gamma interactions
the unique Palphabeta heterodimer contributes to the sophisticated regulation in visual transduction through interaction with Pgamma
although Pgamma-mediated regulation plays the dominant role in visual excitation, the direct, inter-domain allosteric regulation may play a feedback role in light adaptational processes during phototransduction
Retinal degeneration was slowed down in Cngb1/Pde6b double knock-out mice due to lowering of cGMP content in the retinas, and suggests that it may be caused by mislocalization of active Pde6b.
The retinal degeneration (rd) mutant mouse, which carries a genetic mutation of PDE6b.
These results clearly show that the development of early-onset cataracts requires at least two mutant alleles of Foxe3(rct) and Pde6b(rd1), and another modifier associated with the severity of cataract phenotypes in Foxe3(rct) mice underlies the genetic backgrounds in mice.
demonstrated a substantial difference in the speed of retinal degeneration and accompanying loss of visual function between two rd1 lines
transient and Pde6-independent Ca(2+) elevations ('flashes') were detected throughout the inner segment and the synapse.
Polyglutamine expansion AR sequesters PTIP to attenuate DNA repair and increase genomic instability.
There are distinct changes that occur in the morphology of retinal pigment epithelium cells in response to retinal degeneration in rd10 mice.
that effective knockdown of GUCY2E and CNGA1 expression to counteract loss of PDE6 function may develop into a valuable approach for treating some patients with RP.
Phosphodiesterase 6 is involved in the recovery-accelerating effect of red light on the disrupted epidermal permeability barrier.
NC/Tnd mice also preserve the Pde6b(rd1) gene mutation resulting in the rapid postnatal retinal degeneration similar to that in C3H/HeN mice.
Results describe the progression of neuronal remodeling of second- and third-order retinal cells and their synaptic terminals in retinas from Pde6b knockout mice at varying stages of degeneration.
the degeneration of rd1 mouse retina is rescued by antioxidants and involves thiol-dependent metabolism
The main finding of this experiment was the inferior entrainment of rd.rd mice to dim lights.
The differential activation of Akt was studied in the photorceptors of normal and rd1 mice.
These data demonstrate a correlation between genotype and phenotype. Four of the mutants with severe genetic lesions have rapid onset of retinal degeneration, as determined by fundus examination. These mice were indistinguishable from Pde6b(rd1) mice.
In the fear conditioning procedure, the presence of the rd1 mutation had no effect on performance at any stage. In the Morris water maze, only the Pde6b wild-type C3A.BLiA-Pde6b+/J and CBA/CaJ strains were able to demonstrate spatial learning.
H258N mutation in PDE6B causes Congenital Stationary night blindness.
These data demonstrate that P14 (postnatal day 14) administration of AAV5-smCBA-PDEbeta can prevent retinal degeneration in rd10 mice
Pde6b(H620Q) homozygous mice exhibit a hypomorphic phenotype with partial PDE6 activity that may result in an increased Ca(2+) to promote photoreceptor death
Photon absorption triggers a signaling cascade in rod photoreceptors that activates cGMP phosphodiesterase (PDE), resulting in the rapid hydrolysis of cGMP, closure of cGMP-gated cation channels, and hyperpolarization of the cell. PDE is a peripheral membrane heterotrimeric enzyme made up of alpha, beta, and gamma subunits. This gene encodes the beta subunit. Mutations in this gene result in retinitis pigmentosa and autosomal dominant congenital stationary night blindness. Multiple transcript variants encoding different isoforms have been found for this gene.
, rod cGMP-phosphodiesterase beta-subunit
, rod cGMP-specific 3',5'-cyclic phosphodiesterase subunit beta
, pde6B gene for cGMP phosphodiesterase beta subunit
, phosphodiesterase 6B, cGMP-specific, rod, beta (congenital stationary night blindness 3, autosomal dominant)
, rod cGMP phosphodiesterase beta subunit
, phosphodiesterase, cyclic GMP ( rod receptor), beta polypeptide
, phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide
, cGMP-phosphodiesterase beta-subunit
, phosphodiesterase, cGMP, rod receptor, beta polypeptide
, retinal degeneration 1