Axl Antibody [P12M12] | Primary Antibodies

Application: Reactivity: Human, Mouse, Rat

Usage Information

Dilution
WB1:1000 IHC1:400 - 1:1600

Application
WB, IHC

Reactivity
Human, Mouse, Rat

Source
Rabbit Monoclonal Antibody

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
138, 133 kDa

Positive Control	Mouse spleen; Mouse liver; GL261 syngeneic tumor; 4T1 syngeneic mammary tumor; A20 syngeneic tumor; CT26 syngeneic tumor; MC38 syngeneic tumor; MEF cells; C2C12 cells; 3T3-L1 cells; C6 cells; HeLa cells; NIH/3T3 cells
Negative Control	Neuro-2a cells; SK-MEL-28 cells

Datasheet & SDS

Biological Description

Specificity
Axl Antibody [P12M12] detects endogenous levels of total Axl protein.

Clone
P12M12

Synonym(s)
Tyrosine-protein kinase receptor UFO; Adhesion-related kinase; Axl; Ark; Ufo

Background
Axl, also known as AXL receptor tyrosine kinase, is a proto-oncogenic member of the TAM receptor tyrosine kinase family, which includes Sky, also called Tyro3, and Mer. Axl possesses a conserved intracellular tyrosine kinase domain and an extracellular region made up of two immunoglobulin-like domains, IG1 and IG2, along with two fibronectin type III domains, all of which resemble cell adhesion molecules. The primary ligand for Axl is Gas6, or growth-arrest-specific gene 6, a vitamin K-dependent protein that is structurally similar to protein S. In its minimal signaling complex, Gas6 and Axl interact in a 2 to 2 ratio, where the LG1 domain of Gas6 crosslinks the IG1 and IG2 domains of two Axl molecules through both major and minor binding sites. These interactions involve the edge beta strands of Axl, particularly at Glu59 and Thr77, with Arg310 and Lys312 of Gas6, and occur without direct contact between Axl molecules or between Gas6 molecules. This structural arrangement leads to stepwise dimerization, starting with a high-affinity one-to-one binding event and progressing to trans-autophosphorylation of tyrosines inside the cell. The binding of Gas6 to Axl triggers this two-step dimerization, which activates the kinase domain, allowing autophosphorylation and recruitment of proteins with SH2 domains for signal transduction. Among the TAM receptors, Axl exhibits the highest affinity for Gas6, followed by Tyro3 and then Mer. Functionally, Axl is crucial for promoting cell survival, proliferation, migration, and resistance to apoptosis, signaling mainly through the PI3K/Akt/S6K, PLC gamma, Ras/MAPK, and NF-kappaB pathways. Axl also regulates immune responses, platelet aggregation, spermatogenesis, vascular remodeling, and the clearance of apoptotic cells by phagocytes. Gas6/Axl signaling is a major driver of cancer progression, including tumor growth, metastasis, and epithelial-mesenchymal transition in cancers such as non-small cell lung cancer, breast cancer, and glioma. It also contributes to resistance against tyrosine kinase inhibitors and immunotherapy, as well as to inflammation and autoimmune diseases.

Background

Axl, also known as AXL receptor tyrosine kinase, is a proto-oncogenic member of the TAM receptor tyrosine kinase family, which includes Sky, also called Tyro3, and Mer. Axl possesses a conserved intracellular tyrosine kinase domain and an extracellular region made up of two immunoglobulin-like domains, IG1 and IG2, along with two fibronectin type III domains, all of which resemble cell adhesion molecules. The primary ligand for Axl is Gas6, or growth-arrest-specific gene 6, a vitamin K-dependent protein that is structurally similar to protein S. In its minimal signaling complex, Gas6 and Axl interact in a 2 to 2 ratio, where the LG1 domain of Gas6 crosslinks the IG1 and IG2 domains of two Axl molecules through both major and minor binding sites. These interactions involve the edge beta strands of Axl, particularly at Glu59 and Thr77, with Arg310 and Lys312 of Gas6, and occur without direct contact between Axl molecules or between Gas6 molecules. This structural arrangement leads to stepwise dimerization, starting with a high-affinity one-to-one binding event and progressing to trans-autophosphorylation of tyrosines inside the cell. The binding of Gas6 to Axl triggers this two-step dimerization, which activates the kinase domain, allowing autophosphorylation and recruitment of proteins with SH2 domains for signal transduction. Among the TAM receptors, Axl exhibits the highest affinity for Gas6, followed by Tyro3 and then Mer. Functionally, Axl is crucial for promoting cell survival, proliferation, migration, and resistance to apoptosis, signaling mainly through the PI3K/Akt/S6K, PLC gamma, Ras/MAPK, and NF-kappaB pathways. Axl also regulates immune responses, platelet aggregation, spermatogenesis, vascular remodeling, and the clearance of apoptotic cells by phagocytes. Gas6/Axl signaling is a major driver of cancer progression, including tumor growth, metastasis, and epithelial-mesenchymal transition in cancers such as non-small cell lung cancer, breast cancer, and glioma. It also contributes to resistance against tyrosine kinase inhibitors and immunotherapy, as well as to inflammation and autoimmune diseases.

References
https://pubmed.ncbi.nlm.nih.gov/31684958/ https://pubmed.ncbi.nlm.nih.gov/35158733/

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

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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%