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Anti-Phospho-B MyB (Thr487) Rabbit Antibody [B21K19]

Catalog No.: F2054

Application: Reactivity: Human

Usage Information

Dilution
WB1:1000 IHC1:8000 IF1:1000 FCM1:1000

Application
WB, IHC, IF, FCM

Reactivity
Human

Source
Rabbit

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
79 kDa 100 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight.

Positive Control	Human lung cancer tissue; Human colon cancer tissue; HeLa nuclear fraction
Negative Control

Datasheet & SDS

Biological Description

Specificity
Phospho-B MyB (Thr487) Rabbit mAb recognizes endogenous levels of B MyB only when phosphorylated at Thr487.

Clone
B21K19

Synonym(s)
BMYB, MYBL2, Myb-related protein B, B-Myb, Myb-like protein 2

Background
Phospho-B-Myb (Thr487) is a key post-translational modification of the B-Myb transcription factor, which regulates cell cycle progression, DNA repair, and gene expression crucial for cellular proliferation. Phosphorylation at Thr487 occurs in the C-terminal region of B-Myb and plays a pivotal role in modulating its activity in response to DNA damage, such as UV irradiation or genotoxic stress. This modification influences B-Myb's interactions with the MuvB complex, a co-activator involved in cell cycle regulation, and disrupts its association with the MRN complex that governs DNA damage repair. The phosphorylation event leads to a transient recruitment of B-Myb to DNA damage sites, promoting cell cycle checkpoint regulation by reducing the transcriptional activation of pro-mitotic genes like Cyclin B1 and Plk1. The kinase GSK3β is responsible for this phosphorylation, linking it to genotoxic stress responses. Dysregulation of B-Myb, particularly in its phosphorylation status, is associated with several cancers, including breast cancer and leukemia, where overexpression drives uncontrolled proliferation and resistance to chemotherapy.

Background

Phospho-B-Myb (Thr487) is a key post-translational modification of the B-Myb transcription factor, which regulates cell cycle progression, DNA repair, and gene expression crucial for cellular proliferation. Phosphorylation at Thr487 occurs in the C-terminal region of B-Myb and plays a pivotal role in modulating its activity in response to DNA damage, such as UV irradiation or genotoxic stress. This modification influences B-Myb's interactions with the MuvB complex, a co-activator involved in cell cycle regulation, and disrupts its association with the MRN complex that governs DNA damage repair. The phosphorylation event leads to a transient recruitment of B-Myb to DNA damage sites, promoting cell cycle checkpoint regulation by reducing the transcriptional activation of pro-mitotic genes like Cyclin B1 and Plk1. The kinase GSK3β is responsible for this phosphorylation, linking it to genotoxic stress responses. Dysregulation of B-Myb, particularly in its phosphorylation status, is associated with several cancers, including breast cancer and leukemia, where overexpression drives uncontrolled proliferation and resistance to chemotherapy.

References
https://pubmed.ncbi.nlm.nih.gov/22391450/ https://pubmed.ncbi.nlm.nih.gov/28128338/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

Tel: +1-832-582-8158 Ext:3
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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%