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2.5.1.87: ditrans,polycis-polyprenyl diphosphate synthase [(2E,6E)-farnesyl diphosphate specific]

This is an abbreviated version!
For detailed information about ditrans,polycis-polyprenyl diphosphate synthase [(2E,6E)-farnesyl diphosphate specific], go to the full flat file.

Word Map on EC 2.5.1.87

Reaction

(2E,6E)-farnesyl diphosphate
+ n isopentenyl diphosphate = n diphosphate +
ditrans,polycis-polyprenyl diphosphate (n: 10-55)

Synonyms

AcpT, anther-66, cis-prenyltransferase, cis-PTase, CPT1, Dedol-PP synthase, DedolPP synthase, dehydrodolichyl diphosphate synthase, dehydrodolichyl diphosphate synthase 1, DHDDS, NgBR, Nogo-B receptor, RER2, Rer2p, Rer2p Z-prenyltransferase, SlCPT3, SRT1, Srt1p, Srt2p Z-prenyltransferase, Tk-IdsB

ECTree

     2 Transferases
         2.5 Transferring alkyl or aryl groups, other than methyl groups
             2.5.1 Transferring alkyl or aryl groups, other than methyl groups (only sub-subclass identified to date)
                2.5.1.87 ditrans,polycis-polyprenyl diphosphate synthase [(2E,6E)-farnesyl diphosphate specific]

Disease

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Disease on EC 2.5.1.87 - ditrans,polycis-polyprenyl diphosphate synthase [(2E,6E)-farnesyl diphosphate specific]

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DISEASE
TITLE OF PUBLICATION
LINK TO PUBMED
Ataxia
A novel variant of dehydrodolichol diphosphate synthase (DHDDS) mutation with adult-onset progressive myoclonus ataxia.
Blindness
Overexpression and Purification of Human Cis-prenyltransferase in Escherichia coli.
Purification and characterization of human dehydrodolychil diphosphate synthase (DHDDS) overexpressed in E. coli.
Retinal Degeneration Caused by Rod-Specific Dhdds Ablation Occurs without Concomitant Inhibition of Protein N-Glycosylation.
Brain Diseases
De novo DHDDS variants cause a neurodevelopmental and neurodegenerative disorder with myoclonus.
Breast Neoplasms
Nogo-B receptor expression correlates negatively with malignancy grade and ki-67 antigen expression in invasive ductal breast carcinoma.
Nogo-B receptor increases the resistance of estrogen receptor positive breast cancer to paclitaxel.
Nogo-B receptor increases the resistance to tamoxifen in estrogen receptor-positive breast cancer cells.
Carcinogenesis
Nogo-B receptor increases the resistance to tamoxifen in estrogen receptor-positive breast cancer cells.
Research advances on neurite outgrowth inhibitor B receptor.
Carcinoma
Expression of Nogo isoforms and Nogo-B receptor (NgBR) in non-small cell lung carcinomas.
Carcinoma, Hepatocellular
A case of fatal Type I congenital disorders of glycosylation (CDG I) associated with low dehydrodolichol diphosphate synthase (DHDDS) activity.
Nogo-B receptor promotes the chemoresistance of human hepatocellular carcinoma via the ubiquitination of p53 protein.
The Nogo-B receptor promotes human hepatocellular carcinoma cell growth via the Akt signal pathway.
Carcinoma, Non-Small-Cell Lung
Nogo-B receptor is required for stabilizing TGF-? type I receptor and promotes the TGF-?1-induced epithelial-to-mesenchymal transition of non-small cell lung cancer.
Nogo-B receptor promotes epithelial-mesenchymal transition in non-small cell lung cancer cells through the Ras/ERK/Snail1 pathway.
Congenital, Hereditary, and Neonatal Diseases and Abnormalities
Mutation of Nogo-B receptor, a subunit of cis-prenyltransferase, causes a congenital disorder of glycosylation.
ditrans,polycis-polyprenyl diphosphate synthase [(2e,6e)-farnesyl diphosphate specific] deficiency
A case of fatal Type I congenital disorders of glycosylation (CDG I) associated with low dehydrodolichol diphosphate synthase (DHDDS) activity.
Nogo-B receptor deficiency causes cerebral vasculature defects during embryonic development in mice.
Nogo-B receptor deficiency increases liver X receptor alpha nuclear translocation and hepatic lipogenesis through an adenosine monophosphate-activated protein kinase alpha-dependent pathway.
Drug Resistant Epilepsy
Complex Neurological Phenotype Associated with a De Novo DHDDS Mutation in a Boy with Intellectual Disability, Refractory Epilepsy, and Movement Disorder.
Epilepsy, Generalized
A novel variant of dehydrodolichol diphosphate synthase (DHDDS) mutation with adult-onset progressive myoclonus ataxia.
Fifteen-year follow-up of a patient with a DHDDS variant with non-progressive early onset myoclonic tremor and rare generalized epilepsy.
Erectile Dysfunction
Silencing Nogo-B receptor inhibits penile corpus cavernosum vascular smooth muscle cell apoptosis of rats with diabetic erectile dysfunction by down-regulating ICAM-1.
Hyperkinesis
Complex Neurological Phenotype Associated with a De Novo DHDDS Mutation in a Boy with Intellectual Disability, Refractory Epilepsy, and Movement Disorder.
Hypertriglyceridemia
Activation of hepatic Nogo-B receptor expression-A new anti-liver steatosis mechanism of statins.
Intellectual Disability
Complex Neurological Phenotype Associated with a De Novo DHDDS Mutation in a Boy with Intellectual Disability, Refractory Epilepsy, and Movement Disorder.
Lung Neoplasms
Nogo-B receptor is required for stabilizing TGF-? type I receptor and promotes the TGF-?1-induced epithelial-to-mesenchymal transition of non-small cell lung cancer.
Nogo-B receptor promotes epithelial-mesenchymal transition in non-small cell lung cancer cells through the Ras/ERK/Snail1 pathway.
Melanoma
Prognostic Significance of NOGO-A/B and NOGO-B Receptor Expression in Malignant Melanoma - A Preliminary Study.
Movement Disorders
Complex Neurological Phenotype Associated with a De Novo DHDDS Mutation in a Boy with Intellectual Disability, Refractory Epilepsy, and Movement Disorder.
Myoclonus
A novel variant of dehydrodolichol diphosphate synthase (DHDDS) mutation with adult-onset progressive myoclonus ataxia.
De novo DHDDS variants cause a neurodevelopmental and neurodegenerative disorder with myoclonus.
Neoplasm Metastasis
Delivery of small interfering RNA against Nogo-B receptor via tumor-acidity responsive nanoparticles for tumor vessel normalization and metastasis suppression.
Neoplasms
Correlation of Expression of CHI3L1 and Nogo-A and their Role in Angiogenesis in Invasive Ductal Breast Carcinoma.
Delivery of small interfering RNA against Nogo-B receptor via tumor-acidity responsive nanoparticles for tumor vessel normalization and metastasis suppression.
HOXB4 promotes the malignant progression of ovarian cancer via DHDDS.
Nogo-B Receptor Directs Mitochondria-Associated Membranes to Regulate Vascular Smooth Muscle Cell Proliferation.
Nogo-B receptor expression correlates negatively with malignancy grade and ki-67 antigen expression in invasive ductal breast carcinoma.
Neurodegenerative Diseases
De novo DHDDS variants cause a neurodevelopmental and neurodegenerative disorder with myoclonus.
Ovarian Neoplasms
HOXB4 promotes the malignant progression of ovarian cancer via DHDDS.
Retinal Degeneration
Knock-Down DHDDS Expression Induces Photoreceptor Degeneration in Zebrafish.
Knockdown of Dehydrodolichyl Diphosphate Synthase in the Drosophila Retina Leads to a Unique Pattern of Retinal Degeneration.
Lack of Overt Retinal Degeneration in a K42E Dhdds Knock-In Mouse Model of RP59.
Mutation K42E in Dehydrodolichol Diphosphate Synthase (DHDDS) Causes Recessive Retinitis Pigmentosa.
Retinal Degeneration Caused by Rod-Specific Dhdds Ablation Occurs without Concomitant Inhibition of Protein N-Glycosylation.
Selective Ablation of Dehydrodolichyl Diphosphate Synthase in Murine Retinal Pigment Epithelium (RPE) Causes RPE Atrophy and Retinal Degeneration.
Retinal Diseases
Knockdown of Dehydrodolichyl Diphosphate Synthase in the Drosophila Retina Leads to a Unique Pattern of Retinal Degeneration.
Retinitis
De novo DHDDS variants cause a neurodevelopmental and neurodegenerative disorder with myoclonus.
Retinitis Pigmentosa
A missense mutation in DHDDS, encoding dehydrodolichyl diphosphate synthase, is associated with autosomal-recessive retinitis pigmentosa in Ashkenazi Jews.
Aberrant dolichol chain lengths as biomarkers for retinitis pigmentosa caused by impaired dolichol biosynthesis.
De novo DHDDS variants cause a neurodevelopmental and neurodegenerative disorder with myoclonus.
Knockdown of Dehydrodolichyl Diphosphate Synthase in the Drosophila Retina Leads to a Unique Pattern of Retinal Degeneration.
Lack of Overt Retinal Degeneration in a K42E Dhdds Knock-In Mouse Model of RP59.
Mutation K42E in Dehydrodolichol Diphosphate Synthase (DHDDS) Causes Recessive Retinitis Pigmentosa.
Overexpression and Purification of Human Cis-prenyltransferase in Escherichia coli.
Purification and characterization of human dehydrodolychil diphosphate synthase (DHDDS) overexpressed in E. coli.
Retinal Degeneration Caused by Rod-Specific Dhdds Ablation Occurs without Concomitant Inhibition of Protein N-Glycosylation.
Two specific mutations are prevalent causes of recessive retinitis pigmentosa in North American patients of Jewish ancestry.
Whole-exome sequencing links a variant in DHDDS to retinitis pigmentosa.
Seizures
Phenotype of heterozygous variants of dehydrodolichol diphosphate synthase.
Status Epilepticus
Phenotype of heterozygous variants of dehydrodolichol diphosphate synthase.
Tremor
Fifteen-year follow-up of a patient with a DHDDS variant with non-progressive early onset myoclonic tremor and rare generalized epilepsy.