Dynamin-1 Antibodies

Dynamin-1 (DNM1)

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Gene Information

Human
Gene Name:	DNM1
Uniprot:	Q05193
Entrez:	1759

Family

Belongs to:
TRAFAC class dynamin-like GTPase superfamily

Alternative Names

DNM; DNM1; dynamin 1; Dynamin; dynamin-1; EC 3.6.5.5

Molecular Weight

Mass (kDA):
97.408 kDA

Genomic Context

Human
Location:	9q34.11
Sequence:	9; NC_000009.12 (128203379..128255244)

Subcellular Localizations

Cytoplasm. Cytoplasm, cytoskeleton. Microtubule-associated.

Diseases

• Stenosis
• Ataxia
• Muscle Weakness
• Neurodegenerative Disorders
• Nervousness
• Dog Diseases
• Nerve Degeneration
• Optic Atrophy
• Neuromuscular Diseases
• Charcot-marie-tooth Disease
• Intraocular Pressure Disorder
• Atrophy

• Glaucoma
• Serous Endometrial Intraepithelial Carcinoma
• Nicotine Dependence
• Peripheral Neuropathy
• Impaired Cognition
• Friedreich Ataxia
• Nervous System Disorder

Interacting Proteins

• FNBP1
• GRB2
• HTT
• LRRK2
• NCK1

• NOS3
• NOSTRIN
• SNX33
• SNX9

Pathways

• Mitochondrial Fission
• Mitochondrial Fusion
• Localization
• Cell Death
• Endocytosis
• Mating
• Transport
• Aging
• Membrane Fission
• Peroxisome Fission
• Programmed Cell Death
• Cell Cycle
• Clathrin-mediated Endocytosis

• Cytokinesis
• Cell Division
• Pathogenesis
• Oxidative Phosphorylation
• Sporulation
• Synaptic Vesicle Endocytosis
• Rna Interference

PTMs

• Phosphorylation

• Oxidation

Research Areas

• Cell Biology
• Membrane Trafficking and Chaperones
• Neuroscience
• Signal Transduction

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/DNM1

Best Uses Of The DNM1 Marker

Steven Boster was the inventor of his first product in 1993. He earned him the title "he who re-invented science in the lavatory". Since then, he has created a variety of primary antibodies for various applications such as ELISA. Boster was one of China's largest catalog antibody companies in the late 1990s. Boster also developed a unique ELISA platform called PicoKine(tm). This platform allows for the production of highly sensitive ELISA kits.

The use of RNAi therapy to treat DNM1 dee

RNAi gene therapy can mitigate the major impairments that occur in newborn mice suffering from DEEs, including gliosis, cell death, as well as abnormal neuronal metabolic activitythat are associated with recurrent seizures. While it isn't yet tested in humans, the use of RNAi therapy for DEEs may be a potential treatment for these disorders. A new mouse model named Fitful recapitulates the major features of DEE.

RNAi is being developed for various ailments, and DNM1 dee is one of them. It is able of mutating the genes of the disease-causing protein within the brain, and is highly effective in preventing neuronal injury. The most likely candidate for RNAi therapy in the DNM1 case is the altered TA proteins. This treatment method is restricted by its high threshold dose.

The story of Steven Boster's past

Don "Steve" Boster, who passed away on June 6, 2022 in Madison, WI, was born and raised in Joliet, IL. He was a long-standing sales manager. Steve, an U.S. Army veteran was a Concordia Hall member in Staunton, VA. In addition to his wife, Nina Mae, he is survived by 2 daughters - Natosha Peck as well as Crystal Boster - and six grandchildren. His siblings include his wife Frances Boster, Tammy and two sisters, Kimberly Peck, and brother Jack Boster. Steve Boster has several other relatives, including his nieces and nephews.

Steve loved his family more than everything else. His greatest joy and pride was his sons. He was the first to call them when their car broke down in the middle of the night. He even came to rescue them in sub-zero weather! Steve was a fan of sports and auto racing. He was never absent from a race at the local track, and his family would attend other events on weekends. He was a big fan of dirt track racing. He was there, no matter what kind of hot rod or muscle car it was.

Future applications

The most likely biomarker for epileptic diseases is the DNM1 gene. This gene is a highly conserved protein, that functions in synaptic vessel. Mutations in DNM1 could cause Labrador retrievers the syndrome of collapsing after exercise, a life-threatening condition that causes muscle weakness and incoordination. The R256L mutation in the DNM1 gene is the cause of the syndrome. It is seen in a significant proportion of the population of this breed. The DNM1 protein plays a pivotal function in neurotransmission and synaptic endocytosis of the vesicle.

The DNM1 gene is expressed mostly during fetal and adult development. It is most active in the second week postnatally and is the dominant isoform in adulthood. A pathogenic DNM1 variant may be passed down by an asymptomatic parent to a child. The allele is not detected in most cells in cases of mosaic parents. However, a subset cells may have the pathogenic variant, which makes it difficult to determine.

Research has identified several kinds of DNM1 mutations. Different domains of DNM1 result in different clinical symptoms. Epilepticencephalopathy and seizures that are intractable are common symptoms of pathogenic DNM1 variants. Patients with DNM1 mutations may experience severe neurodevelopmental symptoms as well as infantile spasms. Patients suffering from DNM1 mutations may experience various phenotypes, from absence seizures to generalized tonic-clonic seizures.

The DNM1 gene is present throughout the body, including the brain. It was discovered that DNM1 expression is brain by 300% more than elsewhere in the body. The Rat Dnm1 gene is expressed in all tissues, but the amount of DNM1 in the brain is 30 times greater than in the rest of the body. The study also revealed that DNM1 is a particular marker that functions at the nerve terminal of synaptic-vesicle recycling.

The DNM1 gene is an excellent biomarker that could be used to detect CC. It is extremely expressed in breast cancer as well as the ovarian cancer. It is also extremely expressed in other types of cancer. It could be used as a biomarker for CC and aid in predicting the future course of a patient. However, further research is required to confirm these findings. It is crucial to remember that DNM1 expression is associated with the occurrence of cancer.

Genetic testing for DNM1

Although DNM1 is associated with seizures and is often diagnosed through a family history, a genetic test for DNM1 is not necessary for every patient. A third of DNM1 encephalopathy patients have p.Arg237Trp as their most common mutation. Since DNM1 encephalopathy is an extremely homogeneous phenotype as well as a dominant-negative mechanism the gene is a promising therapeutic target. Gene therapy is a promising solution, as it can restore DNM1 function.

One genetic test for DNM1 is the ExAC dataset, which includes variants that were studied in children. The data determines the genes of healthy children as well as the population at large. ExAC data show that 14 out of 20 DNM1 missense mutants were found within the GTPase Domain. DNM1 mutations are typically harmless and do not cause any symptoms. It is worth looking into genetic testing for DNM1 to find a cure.

The genetic testing for DNM1 involves the use of a variety of experiments. The tests were conducted blind to genotype and randomized. The endpoint for adults was PND 30. Typically pups wean between PNDs 22 and 28. Data collection from live mice was stopped when moribundity had been achieved. The study required the use of 80% power to observe the effect. Two F2 hybrid studies were conducted to evaluate the effects of genetic testing for DNM1 dose.

The first genetic connection between DNM1 and epilepsy that is severe was a mutation in the middle domain of DNM1. This mutation encodes peptides necessary to endocytosis, oligomerization and monomerization of the dynamin monomers. Additionally, homozygotes of Dnm1Ftfl/Ftf an ataxia-like DEE phenotype and the development delay. Affected individuals show fully penetrant seizures that can be fatal within the third postnatal week.

The study reveals that there is a p.Arg237Trp mutation is linked to DNM1 disease in 19 sporadic patients as well as one sibling pair. This mutation is unknown and not listed in the gnomAD databank. The most frequently encountered variant in these patients was the Polyphen-2 score 0.988 (p.Arg237Trp). Nine of the 20 patients had frequent mutations.