FGF-2 Polyclonal Antibody
¥680.00
NBR1 Rabbit Polyclonal Antibody
活动价：
¥680.00
市场价：¥880.00
一键复制产品信息
产品规格：
- 50μL
- 100μL
货号：
FAB2607566
- 产品信息
商品描述
靶点-Target
NBR1
反应性
Human,Mouse,Rat
应用
IHC,IF
宿主物种-Host Species
Rabbit
同种型-Isotype
IgG
修饰-Modification
Unmodified
MW(Observed)
120kD
推荐稀释比
IHC 1:50-300;IF 1:50-200
组成
Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
纯化工艺
The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-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
Recombinant Protein of NBR1
特异性
The antibody detects endogenous NBR1 protein
基因名称
NBR1 1A13B KIAA0049 M17S2 MIG19
蛋白名称
Next to BRCA1 gene 1 protein (Cell migration-inducing gene 19 protein) (Membrane component chromosome 17 surface marker 2) (Neighbor of BRCA1 gene 1 protein) (Protein 1A1-3B)
别名
Next to BRCA1 gene 1 protein;Cell migration-inducing gene 19 protein;Membrane component chromosome 17 surface marker 2;Neighbor of BRCA1 gene 1 protein;Protein 1A1-3B;
Organism-1
Human
基因ID-1
4077
SwissProt-1
Q14596
Organism-2
Mouse
SwissProt-2
P97432
Organism-3
Rat
SwissProt-3
Q501R9
背景
The protein encoded by this gene was originally identified as an ovarian tumor antigen monitored in ovarian cancer. The encoded protein contains a B-box/coiled-coil motif, which is present in many genes with transformation potential. It functions as a specific autophagy receptor for the selective autophagic degradation of peroxisomes by forming intracellular inclusions with ubiquitylated autophagic substrates. This gene is located on a region of chromosome 17q21.1 that is in close proximity to the BRCA1 tumor suppressor gene. Alternative splicing of this gene results in multiple transcript variants. [provided by RefSeq, Apr 2014],
细胞定位
Cytoplasm . Cytoplasmic vesicle, autophagosome . Lysosome . Cytoplasm, myofibril, sarcomere, M line . In cardiac muscles localizes to the sarcomeric M line (By similarity). Is targeted to lysosomes for degradation (PubMed:19250911). .
