NDE1 Antibodies

Nuclear distribution protein nudE homolog 1 (NDE1)

Required for centrosome duplication and formation and function of the mitotic spindle. Essential for the growth of the cerebral cortex.

May regulate the production of neurons by controlling the orientation of the mitotic spindle during division of cortical neuronal progenitors of the proliferative ventricular zone of the mind. Orientation of the division plane perpendicular to the layers of the cortex gives rise to two proliferative neuronal progenitors whereas parallel orientation of the division plane yields one proliferative neuronal progenitor and a post- mitotic neuron.

Gene Information

Human
Gene Name:	NDE1
Uniprot:	Q9NXR1
Entrez:	54820

Family

Belongs to:
nudE family

Alternative Names

FLJ20101; HOM-TES-87; nuclear distribution protein nudE homolog 1; nudE nuclear distribution gene E homolog 1 (A. nidulans); NudE; NUDE1; rat homolog

Molecular Weight

Mass (kDA):
37.721 kDA

Genomic Context

Human
Location:	16p13.11
Sequence:	16; NC_000016.10 (15643267..15726353)

Tissue Specificity

Expressed in the neuroepithelium throughout the developing brain, including the cerebral cortex and cerebellum.

Subcellular Localizations

Cytoplasm, cytoskeleton. Cytoplasm, cytoskeleton, microtubule organizing center, centrosome. Chromosome, centromere, kinetochore. Cytoplasm, cytoskeleton, spindle. Cleavage furrow. Localizes to the interphase and S phase centrosome. During mitosis, partially associated with the mitotic spindle. Concentrates at the plus ends of microtubules coincident with kinetochores in metaphase and anaphase in a CENPF-dependent manner. Also localizes to the cleavage furrow during cytokinesis. manner. Also localizes to the cleavage furrow during cytokinesis.

Diseases

• Schizophrenia
• Lissencephaly
• Mental Disorders
• Microcephaly
• Autistic Disorder
• Leukemia
• Malignant Neoplasms
• Neoplasms
• Malignant Paraganglionic Neoplasm
• Depressive Disorder
• Bipolar Disorder
• Microlissencephaly

• Neuronal Migration Disorders
• Congenital Abnormality
• Psychotic Disorders
• Epilepsy
• Haploinsufficiency
• Major Depressive Disorder

Interacting Proteins

• NDEL1
• ZNF365

Pathways

• Mitosis
• Cell Division
• Transport
• Neurogenesis
• Localization
• Electron Transport
• Electron Transport Chain
• Cell Death
• Pathogenesis
• Chromosome Segregation
• Cell Cycle
• Metaphase
• Rna Interference

• Cell Migration
• Tricarboxylic Acid Cycle
• Aging
• Brain Development
• M Phase
• Anaphase
• Cellular Respiration

PTMs

• Phosphorylation
• Oxidation

• Cleavage
• Palmitoylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/NDE1

Best Uses Of The NDE1 Marker

The NDE1 gene is a candidate for a number of applications, including the diagnosis of neurodegenerative diseases. However, the discovery of this gene is controversial. Despite its widespread popularity, the gene is still poorly understood. Its exact location is also unknown. We examined the phenotypes of NDE1 cells to answer these queries. We had to develop a better method to evaluate its potential role as a neurodegenerative factor.

DYRK1A was amplified by PCR

This study identified a single DYRK1A variant that is highly regulated in a variety contexts. In two independent studies, transcription factor E2F1 increased DYRK1A mRNA level. These experiments showed that the activity of the promoter region of this gene was significantly increased by overexpression. The DYRK1A protein is highly regulated and can lead to undesirable consequences in certain situations.

To determine if DYRK1A is necessary for neural specification, hESCs were overexpressed in DYRK1A. In hESCs, increased neural specification is caused by the overexpression of this gene. Induced shRNA inhibition of DYRK1A stops PAX6 induction via dual SMAD inhibition. This offsets the effects caused by DYRK1A high expression. Both reviewers would prefer to see DYRK1A inhibitions be equally effective in more than one huES.

DYRK1A is an alternatively spliced gene in humans. Forward primers were used for amplifying the DYRK1A genome. RT-PCR was used on the first strand cDNA. After the PCR was completed, reaction products were visualized by ethidium Bromide. Lanes 1 through 4 produced PCR products with expected fragment lengths of 192 bp.

DYRK1A mutated mice exhibit pronounced growth retardation and chromosomal heterozygosity, and are homozygous for the mutant gene. The DYRK1A mutation is also due to the Lys188 mutation. Site mutations were used in the construction of siRNA vectors for DYRK1A/KD. GenePharma sold the siRNAs.

DYRK1A is expressed early in chicken embryos. It is found caudally in embryonic development. This gene plays a crucial role in embryonic neurogenesis. It co-expresses MEF2D during neurodevelopment in mice. These co-expressed protein interact with one another and coordinate their expression within the brain.

Down syndrome is thought to be a disorder of the nervous system and is caused by an increase of 1.5-fold in gene dosage in a critical region of the human brain. The human DYRK1A protein is found in significantly more human brains than it was previously thought. In addition to being associated with mental retardation, the gene is also believed to cause brain abnormalities. These diseases could be caused by the gene, according to researchers.

DYRK1A is a complex phosphorylation site and high-expressing in DSCR. In addition to being a component of senile plaques in AD brain, it also has a diverse repertoire of phosphorylation sites. The gene is a useful tool for detecting dementia. These studies also show the potential importance of DYRK1A for AD.

MRD7 development was associated with the mutation of DYRK1A within a Chinese familial. The mutation has enriched our understanding of the mutation spectrum associated with this disorder. Moreover, the study highlights the importance of exome sequencing in identifying MRD7 patients with genetic variants of this gene. Dyregulations in DYRK1A are also affecting many other genes in DS patients.

The sequence of DYRK1A consists of 112 amino acid. The sequence also contains the bipartite nucleotide signal and a short consensus sequence, which are believed to regulate the protein’s activity. ATP binding activity depends on the activity of the first three subdomains within the catalyticdomain. Multiple DYRK1A variants have been identified by molecular analysis.

Three patients' DNA and six control samples were used to sequence the DYRK1A gene Exons. Primers for these regions are listed in Table 3.

The promoter region for DYRK1A includes a MRE site that regulates the expression target genes. The MRE location was located at 268 bp. It is capable in vitro of binding to MEF2D transcription factor. This mutation in DYRK1A leads to a new variant of the gene. Further research is needed to confirm the effects DYRK1A has on MEF2D expression.

Glycogen synase enzyme is believed to be a substrate in DYRK1A. It is also found in many other tissues, including skeletal muscular cells. The regulation of glycogen synthesis is a key function of the DYRK gene family. The regulation of cellular glycogen production is also regulated through the DYRK enzyme. Further studies are needed to determine the role of this enzyme.

DYRK1A and HAN11 are interconnected in Rat-1 fibroblasts. To analyze protein levels, transiently transfected Rat-1 cell lines with DYRK1A gene promoter or HAN11 were used. In COS cells, HAN11-DYRK1A interaction were also studied. Immunoblot was used to identify DYRK1A protein and HAN11 proteins.

In vitro studies have shown that DYRK1A phosphorylates tau at Thr 212, priming it for phosphorylation by GSK3-b at Ser 208. Transgenic mice did not show tau phosphorylation being induced by DYRK1A. However, tau was expressed in greater amounts in transgenic mice. Moreover, DYRK1A is susceptible to dephosphorylation by protein phosphatase-1, which is highly expressed in the frontal lobes.

In addition, Bellmaine et al. Bellmaine et.al. have also included genetic inhibition of DYRK1A to complement pharmacological research. Two simple experiments are still included in the revised manuscript. If the new findings prove valid, this study could lead the development of a novel gene treatment or drug for a wide range human conditions. Activators of DYRK1A, which may be a drug target for ALS, could improve the treatment.

Similarly, chromosome 21, which is associated with an increased likelihood of developing DS, is also linked. The appendicular defects in these mice's bones have been rescued by the reduction of Dyrk1a gene copies in the osteoblasts of mature trisomic mice and euploid mice. Dyregulation of DYRK1A also has an impact on osteoblast cellular functions and morphological parameters. Eventually, this gene can be used to develop a treatment for patients suffering from DS.