ACK Antibody [B23C14] | Primary Antibodies

Application: Reactivity: Mouse, Rat, Human

Usage Information

Dilution
WB1:100- 1:1000 IP1:200-1:400 IF1:50-1:500

Application
WB, IP, IF, ELISA

Reactivity
Mouse, Rat, Human

Source
Mouse 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
60,115,119 kDa

Positive Control	MM-142 cells; EOC 20 cells; HT-1080 cells; HeLa cells; K-562 cells; H4 cells
Negative Control

Datasheet & SDS

Biological Description

Specificity
ACK Antibody [B23C14] detects endogenous levels of total ACK protein.

Clone
B23C14

Synonym(s)
Activated CDC42 kinase 1; ACK-1; Tyrosine kinase non-receptor protein 2; TNK2; ACK1

Background
ACK (Activated Cdc42-Associated Kinase 1, also known as TNK2) is a non-receptor tyrosine kinase of the ACK family that functions as a specific effector for GTP-bound Cdc42, a Rho GTPase crucial for cytoskeletal dynamics, cell migration, and signaling. ACK features a kinase domain adopting an active bilobal conformation independently of phosphorylation at Tyr284, unlike typical kinases that require substantial phosphorylation-dependent activation, flanked by an SH3 domain and a unique C-terminal 47-residue CRIB motif (residues ~850-900), which is essential for high-affinity binding to Cdc42-GTP. Additional domains include SAM and MIG6 interaction sites that facilitate EGFR regulation. ACK inhibits Cdc42 GTPase activity to sustain its active GTP-bound state, thereby promoting Cdc42-mediated actin remodeling, lamellipodia formation, and directional migration. ACK also phosphorylates substrates such as AKT1 (Tyr176, supporting survival signaling), androgen receptor (Tyr267/363, enabling androgen-independent gene activation), WWOX (leading to its ubiquitination and degradation), and WASL, and it integrates into EGFR/clathrin-mediated endocytosis to downregulate receptor signaling while propagating pro-proliferative cues. In Cdc42-dependent pathways, ACK supports cell spreading, survival, and synaptic plasticity, with nuclear translocation enabling AR recruitment to gene enhancers, and biologically, it is implicated in brain development and muscle differentiation through Cdc42 crosstalk. Dysregulated ACK overexpression or amplification is associated with aggressive cancers such as prostate, breast, and gastric tumors, enhancing metastasis, androgen-refractory growth, and chemotherapy resistance.

Background

ACK (Activated Cdc42-Associated Kinase 1, also known as TNK2) is a non-receptor tyrosine kinase of the ACK family that functions as a specific effector for GTP-bound Cdc42, a Rho GTPase crucial for cytoskeletal dynamics, cell migration, and signaling. ACK features a kinase domain adopting an active bilobal conformation independently of phosphorylation at Tyr284, unlike typical kinases that require substantial phosphorylation-dependent activation, flanked by an SH3 domain and a unique C-terminal 47-residue CRIB motif (residues ~850-900), which is essential for high-affinity binding to Cdc42-GTP. Additional domains include SAM and MIG6 interaction sites that facilitate EGFR regulation. ACK inhibits Cdc42 GTPase activity to sustain its active GTP-bound state, thereby promoting Cdc42-mediated actin remodeling, lamellipodia formation, and directional migration. ACK also phosphorylates substrates such as AKT1 (Tyr176, supporting survival signaling), androgen receptor (Tyr267/363, enabling androgen-independent gene activation), WWOX (leading to its ubiquitination and degradation), and WASL, and it integrates into EGFR/clathrin-mediated endocytosis to downregulate receptor signaling while propagating pro-proliferative cues. In Cdc42-dependent pathways, ACK supports cell spreading, survival, and synaptic plasticity, with nuclear translocation enabling AR recruitment to gene enhancers, and biologically, it is implicated in brain development and muscle differentiation through Cdc42 crosstalk. Dysregulated ACK overexpression or amplification is associated with aggressive cancers such as prostate, breast, and gastric tumors, enhancing metastasis, androgen-refractory growth, and chemotherapy resistance.

References
https://pubmed.ncbi.nlm.nih.gov/37194323/ https://pubmed.ncbi.nlm.nih.gov/15308621/

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%