CrkL Antibody - #AF7805

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产品: CrkL 抗体
货号: AF7805
描述: Rabbit polyclonal antibody to CrkL
应用: WB
反应: Human, Mouse, Rat, Monkey
预测: Pig, Zebrafish, Bovine, Horse, Sheep, Rabbit, Dog, Chicken, Xenopus
分子量: 39kDa; 34kD(Calculated).
蛋白号: P46109
RRID: AB_2844169

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产品描述

来源:
Rabbit
应用:
WB 1:500-1:2000
*The optimal dilutions should be determined by the end user.
*Tips:

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:
Human,Mouse,Rat,Monkey
预测:
Pig(100%), Zebrafish(100%), Bovine(100%), Horse(100%), Sheep(100%), Rabbit(100%), Dog(100%), Chicken(100%), Xenopus(100%)
克隆:
Polyclonal
特异性:
CrkL Antibody detects endogenous levels of total CrkL.
RRID:
AB_2844169
引用格式: Affinity Biosciences Cat# AF7805, RRID:AB_2844169.
偶联:
Unconjugated.
纯化:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
保存:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
别名:

展开/折叠

Crk L; Crk like protein; Crk-like protein; Crkl; CRKL_HUMAN; Crkol; HGNC:2363; Oncogene CrkL; V crk avian sarcoma virus CT10 oncogene homolog like; v crk sarcoma virus CT10 oncogene homolog (avian) like; V crk sarcoma virus CT10 oncogene homolog avian like;

抗原和靶标

免疫原:
Uniprot:

P46109(CRKL_HUMAN) >>Visit HPA database.

基因/基因ID:
CRKL(1399)
序列:
MSSARFDSSDRSAWYMGPVSRQEAQTRLQGQRHGMFLVRDSSTCPGDYVLSVSENSRVSHYIINSLPNRRFKIGDQEFDHLPALLEFYKIHYLDTTTLIEPAPRYPSPPMGSVSAPNLPTAEDNLEYVRTLYDFPGNDAEDLPFKKGEILVIIEKPEEQWWSARNKDGRVGMIPVPYVEKLVRSSPHGKHGNRNSNSYGIPEPAHAYAQPQTTTPLPAVSGSPGAAITPLPSTQNGPVFAKAIQKRVPCAYDKTALALEVGDIVKVTRMNINGQWEGEVNGRKGLFPFTHVKIFDPQNPDENE

种属预测

种属预测:

score>80的预测可信度较高，可尝试用于WB检测。*预测模型主要基于免疫原序列比对，结果仅作参考，不作为质保凭据。

Species
Results
Score
Pig
100
Horse
100
Bovine
100
Sheep
100
Dog
100
Xenopus
100
Zebrafish
100
Chicken
100
Rabbit
100
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

翻译修饰 - P46109 作为底物

Site PTM Type Enzyme
R11 Methylation
S41 Phosphorylation
S42 Phosphorylation
T43 Phosphorylation
C44 S-Nitrosylation
Y48 Phosphorylation
Y92 Phosphorylation
T95 Phosphorylation
T96 Phosphorylation
T97 Phosphorylation
S107 Phosphorylation
S112 Phosphorylation
S114 Phosphorylation
Y127 Phosphorylation
T130 Phosphorylation
Y132 Phosphorylation
K145 Ubiquitination
Y177 Phosphorylation
K180 Acetylation
K180 Ubiquitination
S184 Phosphorylation
S185 Phosphorylation
S195 Phosphorylation
S197 Phosphorylation
Y198 Phosphorylation
Y207 Phosphorylation A9UF07 (BCR/ABL fusion) , A0A173G4P4 (Abl fusion) , P00519 (ABL1)
T212 Phosphorylation
T213 Phosphorylation
T214 Phosphorylation
S220 Phosphorylation
S222 Phosphorylation
T228 Phosphorylation
S232 Phosphorylation
Y251 Phosphorylation
K253 Acetylation
K253 Ubiquitination
T254 Phosphorylation
K283 Ubiquitination
K292 Ubiquitination

研究背景

功能:

May mediate the transduction of intracellular signals.

亚基结构:

Interacts with tyrosine-phosphorylated EPOR and INPP5D/SHIP1. Interacts with DOCK2 and DOCK5 via its first SH3 domain. Interacts with phosphorylated CBLB and IRS4.

蛋白家族:

Belongs to the CRK family.

研究领域

· Cellular Processes > Cellular community - eukaryotes > Focal adhesion.   (View pathway)

· Cellular Processes > Cell motility > Regulation of actin cytoskeleton.   (View pathway)

· Environmental Information Processing > Signal transduction > MAPK signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > ErbB signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Rap1 signaling pathway.   (View pathway)

· Human Diseases > Infectious diseases: Bacterial > Bacterial invasion of epithelial cells.

· Human Diseases > Infectious diseases: Bacterial > Shigellosis.

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Cancers: Overview > MicroRNAs in cancer.

· Human Diseases > Cancers: Specific types > Renal cell carcinoma.   (View pathway)

· Human Diseases > Cancers: Specific types > Chronic myeloid leukemia.   (View pathway)

· Organismal Systems > Immune system > Chemokine signaling pathway.   (View pathway)

· Organismal Systems > Immune system > Fc gamma R-mediated phagocytosis.   (View pathway)

· Organismal Systems > Nervous system > Neurotrophin signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Insulin signaling pathway.   (View pathway)

文献引用

1). Silencing of the CrkL gene reverses the doxorubicin resistance of K562/ADR cells through regulating PI3K/Akt/MRP1 signaling. JOURNAL OF CLINICAL LABORATORY ANALYSIS (PubMed: 34114685) [IF=2.7]

Application: WB    Species: Human    Sample: K562/ADR cells

FIGURE 5 Effects of CrkL silencing on nude mice burdened with K562/ADR xenografts. A xenograft tumor model was established via subcutaneously injecting K562/ADR cells. (A) Tumor image was shown in each group. (B-C). The growth curves and weights of the tumors in each group were measured. Silencing CrkL notably inhibited the tumor growth compared with NC group. (D-E) The images of Ki67-IHC were shown in each group and the Ki67 positive staining area was measured. The Ki67 positive staining area of CrkL siRNA treatment was lower compared with the NC group. (F-G) Western blot assay was performed to determine PI3K/AKT/MRP1 pathway-related proteins expression. CrkL silencing in vivo significantly suppressed p-AKT, CrkL, MRP1 protein levels while AKT expression remained unchanged compared with the control and NC groups. The data were represented as mean ± SD of three independent experiments. *p < 0.05, **p < 0.01, ns means not significant, p > 0.05

Application: IHC    Species: Human    Sample: K562/ADR cells

FIGURE 5 Effects of CrkL silencing on nude mice burdened with K562/ADR xenografts. A xenograft tumor model was established via subcutaneously injecting K562/ADR cells. (A) Tumor image was shown in each group. (B-C). The growth curves and weights of the tumors in each group were measured. Silencing CrkL notably inhibited the tumor growth compared with NC group. (D-E) The images of Ki67-IHC were shown in each group and the Ki67 positive staining area was measured. The Ki67 positive staining area of CrkL siRNA treatment was lower compared with the NC group. (F-G) Western blot assay was performed to determine PI3K/AKT/MRP1 pathway-related proteins expression. CrkL silencing in vivo significantly suppressed p-AKT, CrkL, MRP1 protein levels while AKT expression remained unchanged compared with the control and NC groups. The data were represented as mean ± SD of three independent experiments. *p < 0.05, **p < 0.01, ns means not significant, p > 0.05

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