Cortactin Antibody [D8L7] | Primary Antibodies

Application: Reactivity: Mouse, Human

Lane 1: Hela, Lane 2: Hela (KO CTNN), Lane 3: A431, Lane 4: NIH3T3

Usage Information

Dilution
WB1:50000 - 1:100000 IP1:50 IHC1:100 - 1:250 IF1:1000 FCM1:10

Application
WB, IP, IHC, IF, FCM

Reactivity
Mouse, 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
62 kDa 70 kDa, 62 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	Human breast carcinoma; A431 cells; NIH3T3 cells; MCF7 cells; HAP1 cells; HeLa cells; HEK-293T cells
Negative Control

Datasheet & SDS

Biological Description

Specificity
Cortactin Antibody [D8L7] detects endogenous levels of total Cortactin protein.

Clone
D8L7

Synonym(s)
EMS1; CTTN; Src substrate cortactin; Amplaxin; Oncogene EMS1

Background
Cortactin (CTTN) is an actin cytoskeleton regulator overexpressed in the majority of invasive cancers. It contains an N-terminal acidic (NTA) domain with aspartate/glutamate clusters that bind the Arp3 subunit of the Arp2/3 complex, six-and-a-half tandem repeats that form amphipathic helices for high-affinity F-actin crosslinking, a proline-rich region (PRR) with Src-phosphorylatable tyrosines that recruit Nck1/2-SH2 for lamellipodia stabilization, and a C-terminal SH3 domain that interacts with proline motifs in proteins such as N-WASP/WIP (for Arp2/3 branch nucleation), dynamin-2 (for endocytic scission), and Shank3/SANPs (for postsynaptic density and tight junction anchoring). As a class I/II nucleation-promoting factor, cortactin’s NTA domain cooperatively recruits and stabilizes Arp2/3 at branched F-actin networks, while the repeat region crosslinks actin to resist cofilin-mediated debranching, prolonging actin network stability necessary for lamellipodia and endocytic pit function. Tyrosine phosphorylation enhances Arp2/3 activation by relieving N-WASP autoinhibition and integrates with FAK/Src signaling to promote lamellipodin localization. The SH3 domain scaffolds endocytic vesicle scission through dynamin-2 and supports invadopodia maturation via MT1-MMP trafficking and cortactin-MT1 loops, facilitating pericellular matrix proteolysis. Overexpression of cortactin increases invadopodia formation and tumor cell intravasation, especially in head and neck squamous cell carcinoma and breast cancer, correlating with lymph node metastasis and conferring resistance to EGFR-TKIs through FAK pathway bypass.

Background

Cortactin (CTTN) is an actin cytoskeleton regulator overexpressed in the majority of invasive cancers. It contains an N-terminal acidic (NTA) domain with aspartate/glutamate clusters that bind the Arp3 subunit of the Arp2/3 complex, six-and-a-half tandem repeats that form amphipathic helices for high-affinity F-actin crosslinking, a proline-rich region (PRR) with Src-phosphorylatable tyrosines that recruit Nck1/2-SH2 for lamellipodia stabilization, and a C-terminal SH3 domain that interacts with proline motifs in proteins such as N-WASP/WIP (for Arp2/3 branch nucleation), dynamin-2 (for endocytic scission), and Shank3/SANPs (for postsynaptic density and tight junction anchoring). As a class I/II nucleation-promoting factor, cortactin’s NTA domain cooperatively recruits and stabilizes Arp2/3 at branched F-actin networks, while the repeat region crosslinks actin to resist cofilin-mediated debranching, prolonging actin network stability necessary for lamellipodia and endocytic pit function. Tyrosine phosphorylation enhances Arp2/3 activation by relieving N-WASP autoinhibition and integrates with FAK/Src signaling to promote lamellipodin localization. The SH3 domain scaffolds endocytic vesicle scission through dynamin-2 and supports invadopodia maturation via MT1-MMP trafficking and cortactin-MT1 loops, facilitating pericellular matrix proteolysis. Overexpression of cortactin increases invadopodia formation and tumor cell intravasation, especially in head and neck squamous cell carcinoma and breast cancer, correlating with lymph node metastasis and conferring resistance to EGFR-TKIs through FAK pathway bypass.

References
https://pubmed.ncbi.nlm.nih.gov/18406052/ https://pubmed.ncbi.nlm.nih.gov/29152154/

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%