Ataxin-2 Antibody

The autosomal dominant cerebellar ataxias (ADCA) are a heterogeneous group of neurodegenerative disorders characterized by progressive degeneration of the cerebellum, brain stem and spinal cord. Clinically, ADCA has been divided into three groups: ADCA types I-III. ADCAI is genetically heterogeneous, with five genetic loci, designated spinocerebellar ataxia (SCA) 1, 2, 3, 4 and 6, being assigned to five different chromosomes. ADCAII, which always presents with retinal degeneration (SCA7), and ADCAIII often referred to as the `pure' cerebellar syndrome (SCA5), are most likely homogeneous disorders. Several SCA genes have been cloned and shown to contain CAG repeats in their coding regions. ADCA is caused by the expansion of the CAG repeats, producing an elongated polyglutamine tract in the corresponding protein. The expanded repeats are variable in size and unstable, usually increasing in size when transmitted to successive generations. The function of the ataxins is not known. This locus has been mapped to chromosome 12, and it has been determined that the diseased allele contains 36-52 CAG repeats, compared to 22-23 in the normal allele. A potential transcript variant, missing an internal coding exon, has been described; however, its full-length nature is not certain.

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.

We have publications tested in 2 confirmed species: Human, Mouse.

We have publications tested in 2 applications: ICC/IF, WB.

Showing Publications 1 - 6 of 6.

Publications using NBP1-90063	Applications	Species
Qiuyu Martin Zhu, Yu-Han H Hsu, Frederik H Lassen, Bryan T MacDonald, Stephanie Stead, Edyta Malolepsza, April Kim, Taibo Li, Taiji Mizoguchi, Monica Schenone, Gaelen Guzman, Benjamin Tanenbaum, Nadine Fornelos, Steven A Carr, Rajat M Gupta, Patrick T Ellinor, Kasper Lage Protein interaction networks in the vasculature prioritize genes and pathways underlying coronary artery disease. Communications biology 2024-01-15 [PMID: 38216744]
M. Alejandra Zeballos C., Hayden J. Moore, Tyler J. Smith, Jackson E. Powell, Najah S. Ahsan, Sijia Zhang, Thomas Gaj Mitigating a TDP-43 proteinopathy by targeting ataxin-2 using RNA-targeting CRISPR effector proteins Nature Communications 2023-10-14 [PMID: 37838698]
Rodriguez CM, Bechek SC, Jones GL et al. Targeting RTN4/NoGo-Receptor reduces levels of ALS protein ataxin-2 Cell reports 2022-10-25 [PMID: 36288715] (ICC/IF, WB, Human)	ICC/IF, WB	Human
Kim G, Nakayama L, Blum JA et al. Genome-wide CRISPR screen reveals v-ATPase as a drug target to lower levels of ALS protein ataxin-2 Cell reports 2022-10-25 [PMID: 36288714] (ICC/IF, Mouse) Details: Dilution used in ICC 1:1000	ICC/IF	Mouse
Abraham KJ, Chan JN, Salvi JS et al. Intersection of calorie restriction and magnesium in the suppression of genome-destabilizing RNA-DNA hybrids Nucleic Acids Res. 2016-08-29 [PMID: 27574117] (ICC/IF, Human)	ICC/IF	Human
Xia G, Santostefano K, Hamazaki T et al. Generation of Human-Induced Pluripotent Stem Cells to Model Spinocerebellar Ataxia Type 2 In vitro J Mol Neurosci 2012-12-09 [PMID: 23224816] (ICC/IF, WB, Human)	ICC/IF, WB	Human

Array NBP1-90063

• Ataxin-2 Antibodies
• Ataxin-2 ELISA Kits
• Ataxin-2 Proteins