Product: TLR2 Antibody
Catalog: DF7002
Source: Rabbit
Application: WB, IHC, ELISA(peptide)
Reactivity: Human, Mouse, Rat
Prediction: Dog
Mol.Wt.: 90kD; 90kD(Calculated).
Uniprot: O60603
RRID: AB_2838958

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Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200, ELISA(peptide) 1:20000-1:40000
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse,Rat
Prediction:
Dog(83%)
Clonality:
Polyclonal
Specificity:
TLR2 Antibody detects endogenous levels of total TLR2.
RRID:
AB_2838958
Cite Format: Affinity Biosciences Cat# DF7002, RRID:AB_2838958.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
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.
Alias:

Fold/Unfold

CD282; CD282 antigen; TIL 4; TIL4; TLR 2; TLR2; TLR2_HUMAN; Toll like receptor 2; Toll like receptor 2 precursor; Toll-like receptor 2; Toll/interleukin 1 receptor like 4; Toll/interleukin 1 receptor like protein 4; Toll/interleukin receptor like protein 4; Toll/interleukin-1 receptor-like protein 4;

Immunogens

Immunogen:
Uniprot:
Gene(ID):
Expression:
O60603 TLR2_HUMAN:

Highly expressed in peripheral blood leukocytes, in particular in monocytes, in bone marrow, lymph node and in spleen. Also detected in lung and in fetal liver. Levels are low in other tissues.

Description:
Members of the Toll-like receptor (TLR) family, named for the closely related Toll receptor in Drosophila, play a pivotal role in innate immune responses (1-3). TLRs recognize conserved motifs found in various pathogens and mediate defense responses. Triggering of the TLR pathway leads to the activation of NF-κB and subsequent regulation of immune and inflammatory genes. The TLRs and members of the IL-1 receptor family share a conserved stretch of approximately 200 amino acids known as the TIR domain. Upon activation, TLRs associate with a number of cytoplasmic adaptor proteins containing TIR domains including MyD88 (myeloid differentiation factor), MAL/TIRAP (MyD88-adaptor-like/TIR-associated protein), TRIF (Toll-receptor-associated activator of interferon), and TRAM (Toll-receptor-associated molecule). This association leads to the recruitment and activation of IRAK1 and IRAK4, which form a complex with TRAF6 to activate TAK1 and IKK. Activation of IKK leads to the degradation of IκB that normally maintains NF-κB inactivity by sequestering it in the cytoplasm.
Sequence:
MPHTLWMVWVLGVIISLSKEESSNQASLSCDRNGICKGSSGSLNSIPSGLTEAVKSLDLSNNRITYISNSDLQRCVNLQALVLTSNGINTIEEDSFSSLGSLEHLDLSYNYLSNLSSSWFKPLSSLTFLNLLGNPYKTLGETSLFSHLTKLQILRVGNMDTFTKIQRKDFAGLTFLEELEIDASDLQSYEPKSLKSIQNVSHLILHMKQHILLLEIFVDVTSSVECLELRDTDLDTFHFSELSTGETNSLIKKFTFRNVKITDESLFQVMKLLNQISGLLELEFDDCTLNGVGNFRASDNDRVIDPGKVETLTIRRLHIPRFYLFYDLSTLYSLTERVKRITVENSKVFLVPCLLSQHLKSLEYLDLSENLMVEEYLKNSACEDAWPSLQTLILRQNHLASLEKTGETLLTLKNLTNIDISKNSFHSMPETCQWPEKMKYLNLSSTRIHSVTGCIPKTLEILDVSNNNLNLFSLNLPQLKELYISRNKLMTLPDASLLPMLLVLKISRNAITTFSKEQLDSFHTLKTLEAGGNNFICSCEFLSFTQEQQALAKVLIDWPANYLCDSPSHVRGQQVQDVRLSVSECHRTALVSGMCCALFLLILLTGVLCHRFHGLWYMKMMWAWLQAKRKPRKAPSRNICYDAFVSYSERDAYWVENLMVQELENFNPPFKLCLHKRDFIPGKWIIDNIIDSIEKSHKTVFVLSENFVKSEWCKYELDFSHFRLFDENNDAAILILLEPIEKKAIPQRFCKLRKIMNTKTYLEWPMDEAQREGFWVNLRAAIKS

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Dog
83
Horse
78
Pig
74
Bovine
74
Sheep
74
Rabbit
70
Zebrafish
44
Xenopus
0
Chicken
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - O60603 As Substrate

Site PTM Type Enzyme
S45 Phosphorylation
S48 Phosphorylation
N114 N-Glycosylation
T138 Phosphorylation
T142 Phosphorylation
S143 Phosphorylation
S193 Phosphorylation
S196 Phosphorylation
N199 N-Glycosylation
T262 Phosphorylation
Y323 Phosphorylation
N414 N-Glycosylation
N442 N-Glycosylation
Y653 Phosphorylation
K754 Ubiquitination

Research Backgrounds

Function:

Cooperates with LY96 to mediate the innate immune response to bacterial lipoproteins and other microbial cell wall components. Cooperates with TLR1 or TLR6 to mediate the innate immune response to bacterial lipoproteins or lipopeptides. Acts via MYD88 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response. May also activate immune cells and promote apoptosis in response to the lipid moiety of lipoproteins. Recognizes mycoplasmal macrophage-activating lipopeptide-2kD (MALP-2), soluble tuberculosis factor (STF), phenol-soluble modulin (PSM) and B.burgdorferi outer surface protein A lipoprotein (OspA-L) cooperatively with TLR6. Stimulation of monocytes in vitro with M.tuberculosis PstS1 induces p38 MAPK and ERK1/2 activation primarily via this receptor, but also partially via TLR4. MAPK activation in response to bacterial peptidoglycan also occurs via this receptor. Acts as a receptor for M.tuberculosis lipoproteins LprA, LprG, LpqH and PstS1, some lipoproteins are dependent on other coreceptors (TLR1, CD14 and/or CD36); the lipoproteins act as agonists to modulate antigen presenting cell functions in response to the pathogen. M.tuberculosis HSP70 (dnaK) but not HSP65 (groEL-2) acts via this protein to stimulate NF-kappa-B expression. Recognizes M.tuberculosis major T-antigen EsxA (ESAT-6) which inhibits downstream MYD88-dependent signaling (shown in mouse) (By similarity). Forms activation clusters composed of several receptors depending on the ligand, these clusters trigger signaling from the cell surface and subsequently are targeted to the Golgi in a lipid-raft dependent pathway. Forms the cluster TLR2:TLR6:CD14:CD36 in response to diacylated lipopeptides and TLR2:TLR1:CD14 in response to triacylated lipopeptides. Required for normal uptake of M.tuberculosis, a process that is inhibited by M.tuberculosis LppM (By similarity).

PTMs:

Glycosylation of Asn-442 is critical for secretion of the N-terminal ectodomain of TLR2.

Ubiquitinated at Lys-754 by PPP1R11, leading to its degradation. Deubiquitinated by USP2 (By similarity).

Subcellular Location:

Membrane>Single-pass type I membrane protein. Cytoplasmic vesicle>Phagosome membrane>Single-pass type I membrane protein. Membrane raft.
Note: Does not reside in lipid rafts before stimulation but accumulates increasingly in the raft upon the presence of the microbial ligand. In response to diacylated lipoproteins, TLR2:TLR6 heterodimers are recruited in lipid rafts, this recruitment determines the intracellular targeting to the Golgi apparatus. Triacylated lipoproteins induce the same mechanism for TLR2:TLR1 heterodimers.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Highly expressed in peripheral blood leukocytes, in particular in monocytes, in bone marrow, lymph node and in spleen. Also detected in lung and in fetal liver. Levels are low in other tissues.

Subunit Structure:

Interacts with LY96, TLR1 and TLR6 (via extracellular domain). TLR2 seems to exist in heterodimers with either TLR1 or TLR6 before stimulation by the ligand. The heterodimers form bigger oligomers in response to their corresponding ligands as well as further heterotypic associations with other receptors such as CD14 and/or CD36. Binds MYD88 (via TIR domain). Interacts with TICAM1. Interacts with CNPY3 (By similarity). Interacts with ATG16L1. Interacts with PPP1R11 (By similarity). Interacts with TICAM2.

(Microbial infection) Interacts with M.tuberculosis EsxA.

(Microbial infection) Interacts with M.bovis MPB83.

(Microbial infection) Interacts with Staphylococcus aureus protein SSL5.

Family&Domains:

Ester-bound lipid substrates are bound through a crevice formed between the LRR 11 and LRR 12.

The ATG16L1-binding motif mediates interaction with ATG16L1.

The TIR domain mediates NAD(+) hydrolase (NADase) activity. Self-association of TIR domains is required for NADase activity.

Belongs to the Toll-like receptor family.

Research Fields

· Cellular Processes > Transport and catabolism > Phagosome.   (View pathway)

· Environmental Information Processing > Signal transduction > PI3K-Akt signaling pathway.   (View pathway)

· Human Diseases > Infectious diseases: Bacterial > Legionellosis.

· Human Diseases > Infectious diseases: Parasitic > Leishmaniasis.

· Human Diseases > Infectious diseases: Parasitic > Chagas disease (American trypanosomiasis).

· Human Diseases > Infectious diseases: Parasitic > Malaria.

· Human Diseases > Infectious diseases: Parasitic > Toxoplasmosis.

· Human Diseases > Infectious diseases: Parasitic > Amoebiasis.

· Human Diseases > Infectious diseases: Bacterial > Tuberculosis.

· Human Diseases > Infectious diseases: Viral > Hepatitis B.

· Human Diseases > Infectious diseases: Viral > Measles.

· Human Diseases > Infectious diseases: Viral > Herpes simplex infection.

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

· Human Diseases > Immune diseases > Inflammatory bowel disease (IBD).

· Human Diseases > Immune diseases > Rheumatoid arthritis.

· Organismal Systems > Immune system > Toll-like receptor signaling pathway.   (View pathway)

References

1). Yang G et al. A multifunctional anti-inflammatory drug that can specifically target activated macrophages, massively deplete intracellular H2O2, and produce large amounts CO for a highly efficient treatment of osteoarthritis. Biomaterials 2020 Oct;255:120155. (PubMed: 32554130) [IF=15.304]

Application: WB    Species: mouse    Sample: Macrophages

Figure 6. a) CPHs treatment activated the expression of HO-1 in LPS-induced activated macrophages (n = 5), the expression levels of HO-1 in LPS-induced activated macrophages vs that of the free Dex-p, CPs and CPHs treated activated macrophages, b) CPHs treatment downregulated the expression of HO-1, p38, p50, p65 and TLR-2, c-f) Relative p38, p50, p65 and TLR-2 expression level. Free Dex-p and CPs served as control. (n = 3). The relative expression levels of p38, p50, p65 and TLR-2 in LPS-induced activated macrophages vs that of the free Dex-p, CPs and CPHs treated activated macrophages, * p < 0.05, ** p < 0.01, *** p < 0.001.

2). Shen Y et al. Inhibition of murine herpesvirus-68 replication by IFN-gamma in macrophages is counteracted by the induction of SOCS1 expression. PLoS Pathog 2018 Aug 3;14(8):e1007202 (PubMed: 30075008) [IF=7.464]

Application: WB    Species: mouse    Sample: macrophages

Fig 6. |TLR3 mediates the MHV-68-induced SOCS1 production. (A) BMMs were transfected with siRNAs against Tlr2, Tlr3, Tlr4, Tlr7, Tlr9 (si-TLR) or an irrelevant target (si-Control), respectively. Forty-eight hours post transfection, cells were infected with MHV-68 at MOI = 10. At 8 hpi, RNA and protein were then extracted. RT-qPCR was performed to determine SOCS1 mRNA levels and western blotting was performed to determine the protein expression levels of SOCS1 and the individual TLRs, respectively. The SOCS1 mRNA levels are expressed as values relative to the MHV-68 infected, si-Control transfected cells.

3). Wu J et al. Patchouli alcohol attenuates 5-fluorouracil-induced intestinal mucositis via TLR2/MyD88/NF-kB pathway and regulation of microbiota. Biomed Pharmacother 2020 Jan 28;124:109883 (PubMed: 32004938) [IF=7.419]

Application: WB    Species: rat    Sample:

Fig. 3.| Effect of PA on inflammtory cytokines (n = 8) and TLR2/MyD88/NF-κB pathway proteins (n = 3). (a–e) Levels of TNF-α, IL-1β, IL-6, IL-10, and MPO; (f–h)Expressions of TLR2 and MyD88 proteins

4). Wang S et al. 25-HC promotes hepatocellular carcinoma metastasis through up-regulation of TLR4 dependent FABP4. Am J Cancer Res 2019 Oct 1;9(10):2140-2155 (PubMed: 31720079) [IF=5.942]

Application: WB    Species: Human    Sample: HepG2 cells

Figure 5 The migration of HepG2 cells induced by 25-HC is partly mediated by the up-regulation of TLR4. (A) HepG2 cells were treated with the indicated concentrations of 25-HC for 24 hours before mRNA was extracted and expressions of TLR2, TLR4, TLR5, TLR7 and TLR9 were examined by RT-qPCR. (B) HepG2 cells were treated with the indicated concentrations of 25-HC for 24 hours or treated with 25-HC at 10 μM for the indicated times before protein was collected to detect the TLR2, TLR4, TLR5, TLR7 and TLR9 expressions by Western blotting. HepG2 cells were transfected with siNC or siTLR4 or siTLR9 for 24 hours, (C) then cells were treated with the indicated concentrations of 25-HC for 24 hours before proteins were collected and the expressions of MMP1, MMP2, MMP3 and MMP9 were determined by Western blotting. (D) Or migratory ability of HepG2 cells after treated with 25-HC for 36 hours was determined by Transwell assay. Results were obtained from 3 independent experiments and are expressed as the means ± SEM. Statistical significance was determined by Student’s t-test. *P<0.05, ***P<0.001.

5). Wang S et al. 25-HC decreases the sensitivity of human gastric cancer cells to 5-fluorouracil and promotes cells invasion via the TLR2/NF-κB signaling pathway. Int J Oncol 2019 Mar;54(3):966-980 (PubMed: 30664194) [IF=5.884]

6). Cheng Y et al. Novel chimeric TLR2/NOD2 agonist CL429 exhibited significant radioprotective effects in mice. J Cell Mol Med 2021 Apr;25(8):3785-3792. (PubMed: 33609010) [IF=5.295]

Application: WB    Species: Mice    Sample:

FIGURE 5 The mechanism for the radioprotective effect of CL429. (A) C57BL/6 mice and TLR2 KO mice were treated with CL429 before TBI, and then, the survival was monitored (WT n = 11, TLR2 KO n = 7). (B) The representative pathological images of haematopoietic system and gastrointestinal tract at 3.5 d after radiation. (C) The protein expression of TLR2 and NOD2 after siRNA knock‐down. Cell viability was determined using CCK‐8 at 24 h after radiation. *P < .05 vs IR groups. (D) The effects of CL429 on TLR2, NOD2, MyD88 and p‐IKK at 0 h, 2 h, 4 h, 8 h, 12 h and 24 h were measured by Western blot assay. (E) IL‐6, IL‐11, IL‐12 and TNF‐α were detected by ELISA 24 h after radiation. *P < .05, **P < .01 vs IR + PBS groups

7). Tian X et al. Isorhamnetin Ameliorates Aspergillus fumigatus Keratitis by Reducing Fungal Load, Inhibiting Pattern-Recognition Receptors and Inflammatory Cytokines. Invest Ophthalmol Vis Sci 2021 Mar 1;62(3):38. (PubMed: 33783487) [IF=4.925]

Application: WB    Species: Mouse    Sample: RAW264.7 cells

Figure 6. Effects of isorhamnetin on the inflammatory response in A. fumigatus infected mouse cornea. qRT-PCR results for TLR-2 (A), TLR-4 (B), Dectin-1 (C) TNF-α (J) and IL-1β (K) at 1,3, and 5 days p. i. Western blot results and grayscale analysis of TLR-2 (D, G), TLR-4 (E, H), Dectin-1 (F, I) at 3 days p. i. ELISA results of TNF-α (L) and IL-1β (M) at 3 and 5 days p. i. (n = 6 mice/group). All data were mean ± SEM and analyzed by an unpaired, two-tailed Student's t-test.

8). A novel UV-curable extravascular stent to prevent restenosis of venous grafts.

9). The Protective Effect of Artesunate on LPS-Induced Acute Respiratory Distress Syndrome through Inhibiting NLRP3 Inflammasome Signaling.

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