FANCD2 (Phospho Thr691) Rabbit pAb
活动价:
市场价:¥880.00
- 50μL
- 100μL
FAB2612550
- 产品信息
商品描述
靶点-Target
FANCD2
反应性
Human,Mouse,Rat
应用
IHC,WB
宿主物种-Host Species
Rabbit
修饰-Modification
Phospho
MW(Observed)
166kD
推荐稀释比
WB 1:500-2000;IHC 1:50-200
组成
PBS, 50% glycerol, 0.05% Proclin 300, 0.05%BSA
纯化工艺
The antibody was affinity-purified from rabbit serum by affinity-chromatography using specific immunogen.
储存
-15°C to -25°C/1 year(Do not lower than -25°C)
浓度
1 mg/ml
克隆性
Polyclonal
免疫原
Synthesized peptide derived from human FANCD2 (Phospho Thr691)
特异性
This antibody detects endogenous levels of FANCD2 (Phospho Thr691) Rabbit pAb at Human, Mouse,Rat
基因名称
FANCD2 FACD
蛋白名称
Fanconi anemia group D2 protein (Protein FACD2)
别名
Fanconi anemia group D2 protein;Protein FACD2;
Organism-1
Human
基因ID-1
2177
SwissProt-1
Q9BXW9
Organism-2
Mouse
基因ID-2
211651
SwissProt-2
Q80V62
Organism-3
Rat
基因ID-3
312641
SwissProt-3
Q6IV68
背景
Fanconi anemia complementation group D2(FANCD2) Homo sapiens The Fanconi anemia complementation group (FANC) currently includes FANCA, FANCB, FANCC, FANCD1 (also called BRCA2), FANCD2, FANCE, FANCF, FANCG, FANCI, FANCJ (also called BRIP1), FANCL, FANCM and FANCN (also called PALB2). The previously defined group FANCH is the same as FANCA. Fanconi anemia is a genetically heterogeneous recessive disorder characterized by cytogenetic instability, hypersensitivity to DNA crosslinking agents, increased chromosomal breakage, and defective DNA repair. The members of the Fanconi anemia complementation group do not share sequence similarity; they are related by their assembly into a common nuclear protein complex. This gene encodes the protein for complementation group D2. This protein is monoubiquinated in response to DNA damage, resulting in its localization to nuclear foci with other proteins (BRCA1 AND BRCA2) involved in homology-directed DNA repai
细胞定位
Nucleus . Concentrates in nuclear foci during S phase and upon genotoxic stress. At the onset of mitosis, excluded from chromosomes and diffuses into the cytoplasm, returning to the nucleus at the end of cell division. Observed in a few spots localized in pairs on the sister chromatids of mitotic chromosome arms and not centromeres, one on each chromatids. These foci coincide with common fragile sites and could be sites of replication fork stalling. The foci are frequently interlinked through BLM-associated ultra-fine DNA bridges. Following aphidicolin treatment, targets chromatid gaps and breaks.





