Sample type Serum, Plasma, Cell Culture Supernatant, Other liquid samples
Components
Break apart microtiter test strips each coated single wells
8 x 12 (96 Total)
Lyophilized Standard
2 x vial
Biotin-labeled Antibody(Concentrated, 100X)
120 uL
HRP-Streptavidin Conjugate(Concentrated, 100X)
120 uL
Washing solution concentrate (25X)
30 mL
Sample Dilution buffer
20 mL
Antibody Dilution buffer
10 mL
Streptavidin Dilution buffer
10 mL
Stopping solution
10 mL
TMB Substrate (ready-to-use)
10 mL
Plate seals
3
Storage Store at 2-8°C.
target relevance
anti-Tarextumab antibody Anti-drug antibodies (ADAs) generated in subjects following administration of Tarextumab.
Tarextumab Tarextumab biologic drug binds Homo sapiens NOTCH3 Neurogenic locus notch homolog protein 3
Homo sapiens NOTCH3 Neurogenic locus notch homolog protein 3
Protein names Neurogenic locus notch homolog protein 3
Gene names NOTCH3
Protein family Belongs to the NOTCH family
Function Functions as a receptor for membrane-bound ligands Jagged1, Jagged2 and Delta1 to regulate cell-fate determination (PubMed:15350543, PubMed:14714274). Upon ligand activation through the released notch intracellular domain (NICD), it forms a transcriptional activator complex with RBPJ/RBPSUH and activates genes of the enhancer of split locus. Affects the implementation of differentiation, proliferation and apoptotic programs (By similarity)
Subcellular location Nucleus
Structure Heterodimer of a C-terminal fragment N(TM) and a N-terminal fragment N(EC) which are probably linked by disulfide bonds (PubMed:19417009). Interacts with MAML1, MAML2 and MAML3 which act as transcriptional coactivators for NOTCH3. Interacts with PSMA1. Interacts with HIF1AN
Post-translational modification Synthesized in the endoplasmic reticulum as an inactive form which is proteolytically cleaved by a furin-like convertase in the trans-Golgi network before it reaches the plasma membrane to yield an active, ligand-accessible form. Cleavage results in a C-terminal fragment N(TM) and a N-terminal fragment N(EC). Following ligand binding, it is cleaved by TNF converting enzyme (TACE) to yield a membrane-associated intermediate fragment called notch extracellular truncation (NEXT). This fragment is then cleaved by presenilin dependent gamma-secretase to release a notch-derived peptide containing the intracellular domain (NICD) from the membrane Phosphorylated Hydroxylated by HIF1AN
Involvement in disease Cerebral arteriopathy, autosomal dominant, with subcortical infarcts and leukoencephalopathy, 1 A cerebrovascular disease characterized by multiple subcortical infarcts, pseudobulbar palsy, dementia, and the presence of granular deposits in small cerebral arteries producing ischemic stroke.
Cerebral arteriopathy, autosomal recessive, with subcortical infarcts and leukoencephalopathy 1 A cerebrovascular disease characterized by arteriopathy of cerebral small vessels and onset of neurologic symptoms in infancy or early childhood. Affected individuals present with periventricular or periatrial leukoencephalopathy, white matter lesions in the basal ganglia, microbleeds, enlarged ventricles, and white matter volume loss. Additional features include hypotonia, developmental delay, variably impaired intellectual development, spasticity, hyperreflexia, stoke, hemiparesis, seizures, coarse facial features, and strabismus.
Myofibromatosis, infantile 2 A rare mesenchymal disorder characterized by the development of benign tumors in the skin, striated muscles, bones, and, more rarely, visceral organs. Subcutaneous or soft tissue nodules commonly involve the skin of the head, neck, and trunk. Skeletal and muscular lesions occur in about half of the patients. Lesions may be solitary or multicentric, and they may be present at birth or become apparent in early infancy or occasionally in adult life. Visceral lesions are associated with high morbidity and mortality.
Lateral meningocele syndrome A very rare skeletal disorder with facial anomalies, hypotonia and neurologic dysfunction due to meningocele, a protrusion of the meninges, unaccompanied by neural tissue, through a bony defect in the skull or vertebral column. LMNS facial features include hypertelorism and telecanthus, high arched eyebrows, ptosis, mid-facial hypoplasia, micrognathia, high and narrow palate, low-set ears and a hypotonic appearance. Additional variable features are connective tissue abnormalities, aortic dilation, a high-pitched nasal voice, wormian bones and osteolysis.
Lipodystrophy, familial partial, 1 A form of partial lipodystrophy, a disorder characterized by abnormal subcutaneous fat distribution. FPLD1 affected individuals have loss of subcutaneous adipose tissue from the upper and lower extremities, increased muscularity, and normal or increased distribution of fat in the trunk or abdomen. Patients develop metabolic complications including hypertriglyceridemia, hepatic steatosis, and insulin-dependent diabetes. FPLD1 is an autosomal dominant disorder with age-dependent penetrance.
We haven't added any publications to our database yet.
Published literature highly relevant to the biological target of this product and referencing this antibody or clone are retrieved from the PubMed database provided by the United States National Library of Medicine at the National Institutes of Health.
Reviews
There are no reviews yet.