CBL C-terminal Antibody [A13K3] | Primary Antibodies

Application: Reactivity: Mouse, Rat, Human

Lane 1: Raji, Lane 2: Mouse thymus, Lane 3: Rat testis, Lane 4: Rat thymus

Usage Information

Dilution
WB1:1000 IF1:50 FCM1:30

Application
WB, IF, FCM

Reactivity
Mouse, Rat, Human

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 Observed MW
100 kDa 105-110 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	Mouse thymus; Rat testis; Rat thymus; Jurkat cells; WEHI-231 cells; HAP1 cells; F9 cells; HCT 116 cells; HEK293T cells; Raji cells; THP-1 cells
Negative Control	NIH/3T3 cells

Datasheet & SDS

Biological Description

Specificity
CBL C-terminal Antibody [A13K3] detects endogenous levels of C-terminal of total CBL protein.

Clone
A13K3

Synonym(s)
CBL2; RNF55; CBL; E3 ubiquitin-protein ligase CBL; Casitas B-lineage lymphoma proto-oncogene; Proto-oncogene c-Cbl; RING finger protein 55; RING-type E3 ubiquitin transferase CBL; Signal transduction protein CBL

Background
The CBL C-terminal region is a multifunctional adaptor module that plays a pivotal role in regulating receptor tyrosine kinase (RTK) signaling and cellular homeostasis. This segment features proline-rich regions that engage SH3 domain-containing proteins, tyrosine-rich motifs that serve as SH2-binding sites upon phosphorylation, and a ubiquitin-associated (UBA) domain with conserved hydrophobic patches that recognize mono- and polyubiquitin chains. Through these structural elements, the CBL C-terminus orchestrates the assembly of signaling complexes and modulates E3 ubiquitin ligase activity by facilitating interactions with regulatory proteins such as CIN85, Endophilin, and PI3K/p85, and by recruiting ubiquitinated substrates for proteasomal degradation. The UBA domain can autoinhibit the N-terminal RING ligase domain via intramolecular masking, which is relieved upon phosphorylation of key tyrosine residues, enabling efficient E2~Ub recruitment and RTK polyubiquitination. This tightly regulated process ensures timely signal attenuation, endocytosis, and lysosomal trafficking of activated RTKs, preventing excessive downstream MAPK and PI3K pathway activation. Pathogenic deletions or mutations within the CBL C-terminal region disrupt these feedback mechanisms, leading to aberrant RTK signaling and are implicated in disorders such as Noonan syndrome, juvenile myelomonocytic leukemia, and acute myeloid leukemia.

Background

The CBL C-terminal region is a multifunctional adaptor module that plays a pivotal role in regulating receptor tyrosine kinase (RTK) signaling and cellular homeostasis. This segment features proline-rich regions that engage SH3 domain-containing proteins, tyrosine-rich motifs that serve as SH2-binding sites upon phosphorylation, and a ubiquitin-associated (UBA) domain with conserved hydrophobic patches that recognize mono- and polyubiquitin chains. Through these structural elements, the CBL C-terminus orchestrates the assembly of signaling complexes and modulates E3 ubiquitin ligase activity by facilitating interactions with regulatory proteins such as CIN85, Endophilin, and PI3K/p85, and by recruiting ubiquitinated substrates for proteasomal degradation. The UBA domain can autoinhibit the N-terminal RING ligase domain via intramolecular masking, which is relieved upon phosphorylation of key tyrosine residues, enabling efficient E2~Ub recruitment and RTK polyubiquitination. This tightly regulated process ensures timely signal attenuation, endocytosis, and lysosomal trafficking of activated RTKs, preventing excessive downstream MAPK and PI3K pathway activation. Pathogenic deletions or mutations within the CBL C-terminal region disrupt these feedback mechanisms, leading to aberrant RTK signaling and are implicated in disorders such as Noonan syndrome, juvenile myelomonocytic leukemia, and acute myeloid leukemia.

References
https://pubmed.ncbi.nlm.nih.gov/9720760/ https://pubmed.ncbi.nlm.nih.gov/11607840/

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%