Key Specifications Table
|Species Reactivity||Key Applications||Host||Format||Antibody Type|
|H||IF, IP, WB||M||Purified||Monoclonal Antibody|
|Presentation||0.05M Potassium phosphate, 0.3M Sodium chloride, and 0.05% Sodium azide|
|Safety Information according to GHS|
|Storage and Shipping Information|
|Storage Conditions||Maintain at 2-8°C for up 12 months from date of receipt.|
|Material Size||100 µg|
|MOUSE ANTI-B23 MONOCLONAL ANTIBODY - 2092686||2092686|
|MOUSE ANTI-B23 MONOCLONAL ANTIBODY - 2135104||2135104|
|MOUSE ANTI-B23 MONOCLONAL ANTIBODY - 2433381||2433381|
|MOUSE ANTI-B23 -2717668||2717668|
|MOUSE ANTI-B23 -2733579||2733579|
|MOUSE ANTI-B23 -2738432||2738432|
|MOUSE ANTI-B23 MONOCLONAL ANTIBODY - 1983680||1983680|
|MOUSE ANTI-B23 MONOCLONAL ANTIBODY - 2318787||2318787|
|Reference overview||Application||Pub Med ID|
|Major differences between tumor and normal human cell fates after exposure to chemotherapeutic monofunctional alkylator. |
Gupte, M; Tuck, AN; Sharma, VP; Williams, KJ
PloS one 8 e74071 2013
The major dilemma of cancer chemotherapy has always been a double-edged sword, producing resistance in tumor cells and life-threatening destruction of nontumorigenic tissue. Glioblastoma is the most common form of primary brain tumor, with median survival at 14 months after surgery, radiation and temozolomide (monofunctional alkylator) therapy. Treatment failure is most often due to temozolomide-resistant tumor growth. The underlying basis for development of tumor cell resistance to temozolomide instead of death is not understood. Our current results demonstrate that both cervical carcinoma (HeLa MR) and glioblastoma (U251) tumor cells exposed to an equivalent chemotherapeutic concentration of a monofunctional alkylator undergo multiple cell cycles, maintenance of metabolic activity, and a prolonged time to death that involves accumulation of Apoptosis Inducing Factor (AIF) within the nucleus. A minority of the tumor cell population undergoes senescence, with minimal caspase cleavage. Surviving tumor cells are comprised of a very small subpopulation of individual cells that eventually resume proliferation, out of which resistant cells emerge. In contrast, normal human cells (MCF12A) exposed to a monofunctional alkylator undergo an immediate decrease in metabolic activity and subsequent senescence. A minority of the normal cell population undergoes cell death by the caspase cleavage pathway. All cytotoxic events occur within the first cell cycle in nontumorigenic cells. In summation, we have demonstrated that two different highly malignant tumor cell lines slowly undergo very altered cellular and temporal responses to chemotherapeutic monofunctional alkylation, as compared to rapid responses of normal cells. In the clinic, this produces resistance and growth of tumor cells, cytotoxicity of normal cells, and death of the patient.
|ATRX-mediated chromatin association of histone variant macroH2A1 regulates α-globin expression. |
Ratnakumar, K; Duarte, LF; LeRoy, G; Hasson, D; Smeets, D; Vardabasso, C; Bönisch, C; Zeng, T; Xiang, B; Zhang, DY; Li, H; Wang, X; Hake, SB; Schermelleh, L; Garcia, BA; Bernstein, E
Genes & development 26 433-8 2012
The histone variant macroH2A generally associates with transcriptionally inert chromatin; however, the factors that regulate its chromatin incorporation remain elusive. Here, we identify the SWI/SNF helicase ATRX (α-thalassemia/MR, X-linked) as a novel macroH2A-interacting protein. Unlike its role in assisting H3.3 chromatin deposition, ATRX acts as a negative regulator of macroH2A's chromatin association. In human erythroleukemic cells deficient for ATRX, macroH2A accumulates at the HBA gene cluster on the subtelomere of chromosome 16, coinciding with the loss of α-globin expression. Collectively, our results implicate deregulation of macroH2A's distribution as a contributing factor to the α-thalassemia phenotype of ATRX syndrome.
|BRCA2 and nucleophosmin coregulate centrosome amplification and form a complex with the Rho effector kinase ROCK2. |
Wang, HF; Takenaka, K; Nakanishi, A; Miki, Y
Cancer research 71 68-77 2011
BRCA2 germline mutations account for the majority of heredity breast and ovarian cancer. Besides its role in DNA damage repair, BRCA2 also plays an important role in cytokinesis, transcription regulation, and cancer cell proliferation. Recently, we reported that BRCA2 localizes to centrosomes as well as nuclei and the dysfunction of BRCA2 in a centrosome causes abnormalities in cell division. Here, we identified a nucleolar phosphoprotein, nucleophosmin (NPM), as a novel BRCA2-associated protein. We also detected the binding of BRCA2 to ROCK2, an effector of Rho small GTPase. Because it is known that ROCK2 binds to NPM at centrosomes, these 3 proteins may form a complex. NPM-binding region was within amino acids 639-1,000 of BRCA2. Exogenous expression of this BRCA2 region resulted in aberrant centrosome amplification and a high frequency of multinucleated cells. Our results suggested that a complex consisting of BRCA2, NPM, and ROCK2 maintains the numerical integrity of centrosomes and accurate cell division and that dysfunction of this regulation might be involved in the tumorigenesis of breast cancer.
|Nucleolar disruption in dopaminergic neurons leads to oxidative damage and parkinsonism through repression of mammalian target of rapamycin signaling. |
Rieker, C; Engblom, D; Kreiner, G; Domanskyi, A; Schober, A; Stotz, S; Neumann, M; Yuan, X; Grummt, I; Schütz, G; Parlato, R
The Journal of neuroscience : the official journal of the Society for Neuroscience 31 453-60 2011
The nucleolus represents an essential stress sensor for the cell. However, the molecular consequences of nucleolar damage and their possible link with neurodegenerative diseases remain to be elucidated. Here, we show that nucleolar damage is present in both genders in Parkinson's disease (PD) and in the pharmacological PD model induced by the neurotoxin 1,2,3,6-tetrahydro-1-methyl-4-phenylpyridine hydrochloride (MPTP). Mouse mutants with nucleolar disruption restricted to dopaminergic (DA) neurons show phenotypic alterations that resemble PD, such as progressive and differential loss of DA neurons and locomotor abnormalities. At the molecular level, nucleolar disruption results in increased p53 levels and downregulation of mammalian target of rapamycin (mTOR) activity, leading to mitochondrial dysfunction and increased oxidative stress, similar to PD. In turn, increased oxidative stress induced by MPTP causes mTOR and ribosomal RNA synthesis inhibition. Collectively, these observations suggest that the interplay between nucleolar dysfunction and increased oxidative stress, involving p53 and mTOR signaling, may constitute a destructive axis in experimental and sporadic PD.
|Pten ablation in adult dopaminergic neurons is neuroprotective in Parkinson's disease models. |
Domanskyi, A; Geissler, C; Vinnikov, IA; Alter, H; Schober, A; Vogt, MA; Gass, P; Parlato, R; Schütz, G
FASEB journal : official publication of the Federation of American Societies for Experimental Biology 25 2898-910 2011
Parkinson's disease (PD) is a progressive age-related movement disorder that results primarily from the selective loss of midbrain dopaminergic (DA) neurons. Symptoms of PD can be induced by genetic mutations or by DA neuron-specific toxins. A specific ablation of an essential factor controlling ribosomal RNA transcription, TifIa, in adult mouse DA neurons represses mTOR signaling and leads to progressive neurodegeneration and PD-like phenotype. Using an inducible Cre system in adult mice, we show here that the specific ablation of Pten in adult mouse DA neurons leads to activation of mTOR pathway and is neuroprotective in genetic (TifIa deletion) and neurotoxin-induced (MPTP or 6OHDA) mouse models of PD. Adult mice with DA neuron-specific Pten deletion exhibit elevated expression of tyrosine hydroxylase, a rate-limiting enzyme in the dopamine biosynthesis pathway, associated with increased striatal dopamine content, and increased mRNA levels of Foxa2, Pitx3, En1, Nurr1, and Lmx1b-the essential factors for maintaining physiological functions of adult DA neurons. Pten deletion attenuates the loss of tyrosine hydroxylase-positive cells after 6OHDA treatment, restores striatal dopamine in TifIa-knockout and MPTP-treated mice, and rescues locomotor impairments caused by TifIa loss. Inhibition of Pten-dependent functions in adult DA neurons may represent a promising PD therapy.
|Anti-B23, clone 3C9 - Data Sheet|