Product: Cleaved-Notch 1 (Val1744) Antibody
Catalog: AF5307
Description: Rabbit polyclonal antibody to Cleaved-Notch 1 (Val1744)
Application: WB IHC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Bovine, Horse, Dog
Mol.Wt.: 95 kDa; 273kD(Calculated).
Uniprot: P46531
RRID: AB_2837792

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Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200
*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:
Pig(100%), Bovine(100%), Horse(100%), Dog(100%)
Clonality:
Polyclonal
Specificity:
Cleaved-Notch 1 (Val1744) Antibody detects endogenous levels of fragment of activated Notch 1 resulting from cleavage adjacent to Val1744.
RRID:
AB_2837792
Cite Format: Affinity Biosciences Cat# AF5307, RRID:AB_2837792.
Conjugate:
Unconjugated.
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

9930111A19Rik; AOS5; AOVD1; hN1; Lin-12; LIN12; Mis6; Motch A; mT14; Neurogenic locus notch homolog protein 1; Neurogenic locus notch protein homolog; NICD; NOTC1_HUMAN; Notch 1; Notch 1 intracellular domain; NOTCH; Notch gene homolog 1 (Drosophila); Notch homolog 1, translocation-associated (Drosophila); NOTCH, Drosophila, homolog of, 1; notch1; TAN1; Translocation associated notch homolog; Translocation associated notch protein TAN 1; Translocation-associated notch protein TAN-1; xotch;

Immunogens

Immunogen:
Uniprot:
Gene(ID):
Expression:
P46531 NOTC1_HUMAN:

In fetal tissues most abundant in spleen, brain stem and lung. Also present in most adult tissues where it is found mainly in lymphoid tissues.

Description:
Functions as a receptor for membrane-bound ligands Jagged1, Jagged2 and Delta1 to regulate cell-fate determination. Upon ligand activation through the released notch intracellular domain (NICD) it forms a transcriptional activator complex with RBPJ/RBPSUH and activates genes of the enhancer of split locus
Sequence:
MPPLLAPLLCLALLPALAARGPRCSQPGETCLNGGKCEAANGTEACVCGGAFVGPRCQDPNPCLSTPCKNAGTCHVVDRRGVADYACSCALGFSGPLCLTPLDNACLTNPCRNGGTCDLLTLTEYKCRCPPGWSGKSCQQADPCASNPCANGGQCLPFEASYICHCPPSFHGPTCRQDVNECGQKPGLCRHGGTCHNEVGSYRCVCRATHTGPNCERPYVPCSPSPCQNGGTCRPTGDVTHECACLPGFTGQNCEENIDDCPGNNCKNGGACVDGVNTYNCRCPPEWTGQYCTEDVDECQLMPNACQNGGTCHNTHGGYNCVCVNGWTGEDCSENIDDCASAACFHGATCHDRVASFYCECPHGRTGLLCHLNDACISNPCNEGSNCDTNPVNGKAICTCPSGYTGPACSQDVDECSLGANPCEHAGKCINTLGSFECQCLQGYTGPRCEIDVNECVSNPCQNDATCLDQIGEFQCICMPGYEGVHCEVNTDECASSPCLHNGRCLDKINEFQCECPTGFTGHLCQYDVDECASTPCKNGAKCLDGPNTYTCVCTEGYTGTHCEVDIDECDPDPCHYGSCKDGVATFTCLCRPGYTGHHCETNINECSSQPCRHGGTCQDRDNAYLCFCLKGTTGPNCEINLDDCASSPCDSGTCLDKIDGYECACEPGYTGSMCNINIDECAGNPCHNGGTCEDGINGFTCRCPEGYHDPTCLSEVNECNSNPCVHGACRDSLNGYKCDCDPGWSGTNCDINNNECESNPCVNGGTCKDMTSGYVCTCREGFSGPNCQTNINECASNPCLNQGTCIDDVAGYKCNCLLPYTGATCEVVLAPCAPSPCRNGGECRQSEDYESFSCVCPTGWQGQTCEVDINECVLSPCRHGASCQNTHGGYRCHCQAGYSGRNCETDIDDCRPNPCHNGGSCTDGINTAFCDCLPGFRGTFCEEDINECASDPCRNGANCTDCVDSYTCTCPAGFSGIHCENNTPDCTESSCFNGGTCVDGINSFTCLCPPGFTGSYCQHDVNECDSQPCLHGGTCQDGCGSYRCTCPQGYTGPNCQNLVHWCDSSPCKNGGKCWQTHTQYRCECPSGWTGLYCDVPSVSCEVAAQRQGVDVARLCQHGGLCVDAGNTHHCRCQAGYTGSYCEDLVDECSPSPCQNGATCTDYLGGYSCKCVAGYHGVNCSEEIDECLSHPCQNGGTCLDLPNTYKCSCPRGTQGVHCEINVDDCNPPVDPVSRSPKCFNNGTCVDQVGGYSCTCPPGFVGERCEGDVNECLSNPCDARGTQNCVQRVNDFHCECRAGHTGRRCESVINGCKGKPCKNGGTCAVASNTARGFICKCPAGFEGATCENDARTCGSLRCLNGGTCISGPRSPTCLCLGPFTGPECQFPASSPCLGGNPCYNQGTCEPTSESPFYRCLCPAKFNGLLCHILDYSFGGGAGRDIPPPLIEEACELPECQEDAGNKVCSLQCNNHACGWDGGDCSLNFNDPWKNCTQSLQCWKYFSDGHCDSQCNSAGCLFDGFDCQRAEGQCNPLYDQYCKDHFSDGHCDQGCNSAECEWDGLDCAEHVPERLAAGTLVVVVLMPPEQLRNSSFHFLRELSRVLHTNVVFKRDAHGQQMIFPYYGREEELRKHPIKRAAEGWAAPDALLGQVKASLLPGGSEGGRRRRELDPMDVRGSIVYLEIDNRQCVQASSQCFQSATDVAAFLGALASLGSLNIPYKIEAVQSETVEPPPPAQLHFMYVAAAAFVLLFFVGCGVLLSRKRRRQHGQLWFPEGFKVSEASKKKRREPLGEDSVGLKPLKNASDGALMDDNQNEWGDEDLETKKFRFEEPVVLPDLDDQTDHRQWTQQHLDAADLRMSAMAPTPPQGEVDADCMDVNVRGPDGFTPLMIASCSGGGLETGNSEEEEDAPAVISDFIYQGASLHNQTDRTGETALHLAARYSRSDAAKRLLEASADANIQDNMGRTPLHAAVSADAQGVFQILIRNRATDLDARMHDGTTPLILAARLAVEGMLEDLINSHADVNAVDDLGKSALHWAAAVNNVDAAVVLLKNGANKDMQNNREETPLFLAAREGSYETAKVLLDHFANRDITDHMDRLPRDIAQERMHHDIVRLLDEYNLVRSPQLHGAPLGGTPTLSPPLCSPNGYLGSLKPGVQGKKVRKPSSKGLACGSKEAKDLKARRKKSQDGKGCLLDSSGMLSPVDSLESPHGYLSDVASPPLLPSPFQQSPSVPLNHLPGMPDTHLGIGHLNVAAKPEMAALGGGGRLAFETGPPRLSHLPVASGTSTVLGSSSGGALNFTVGGSTSLNGQCEWLSRLQSGMVPNQYNPLRGSVAPGPLSTQAPSLQHGMVGPLHSSLAASALSQMMSYQGLPSTRLATQPHLVQTQQVQPQNLQMQQQNLQPANIQQQQSLQPPPPPPQPHLGVSSAASGHLGRSFLSGEPSQADVQPLGPSSLAVHTILPQESPALPTSLPSSLVPPVTAAQFLTPPSQHSYSSPVDNTPSHQLQVPEHPFLTPSPESPDQWSSSSPHSNVSDWSEGVSSPPTSMQSQIARIPEAFK

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
Pig
100
Horse
100
Bovine
100
Dog
100
Sheep
0
Xenopus
0
Zebrafish
0
Chicken
0
Rabbit
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - P46531 As Substrate

Site PTM Type Enzyme
T232 O-Glycosylation
S435 O-Glycosylation
S900 Phosphorylation
K1317 Acetylation
T1402 O-Glycosylation
T1725 O-Glycosylation
S1791 Phosphorylation
K1795 Ubiquitination
S1801 Phosphorylation
K1821 Ubiquitination
T1861 Phosphorylation
T1897 Phosphorylation
S1900 Phosphorylation P68400 (CSNK2A1)
T1927 Phosphorylation
T1930 Phosphorylation
S1941 Phosphorylation
R1946 Methylation
S1951 Phosphorylation
T1986 Phosphorylation
T1996 Phosphorylation
T1997 Phosphorylation
Y2074 Phosphorylation
T2090 Phosphorylation
S2121 Phosphorylation
S2136 Phosphorylation
Y2145 Phosphorylation
S2148 Phosphorylation
K2157 Acetylation
K2160 Acetylation
S2162 Phosphorylation
K2164 Acetylation
K2171 Acetylation
K2174 Acetylation
Y2323 Phosphorylation
T2511 Phosphorylation
S2513 Phosphorylation
S2516 Phosphorylation
S2521 Phosphorylation
S2522 Phosphorylation
S2523 Phosphorylation
S2524 Phosphorylation

Research Backgrounds

Function:

Functions as a receptor for membrane-bound ligands Jagged-1 (JAG1), Jagged-2 (JAG2) and Delta-1 (DLL1) to regulate cell-fate determination. Upon ligand activation through the released notch intracellular domain (NICD) it forms a transcriptional activator complex with RBPJ/RBPSUH and activates genes of the enhancer of split locus. Affects the implementation of differentiation, proliferation and apoptotic programs. Involved in angiogenesis; negatively regulates endothelial cell proliferation and migration and angiogenic sprouting. Involved in the maturation of both CD4(+) and CD8(+) cells in the thymus. Important for follicular differentiation and possibly cell fate selection within the follicle. During cerebellar development, functions as a receptor for neuronal DNER and is involved in the differentiation of Bergmann glia. Represses neuronal and myogenic differentiation. May play an essential role in postimplantation development, probably in some aspect of cell specification and/or differentiation. May be involved in mesoderm development, somite formation and neurogenesis. May enhance HIF1A function by sequestering HIF1AN away from HIF1A. Required for the THBS4 function in regulating protective astrogenesis from the subventricular zone (SVZ) niche after injury. Involved in determination of left/right symmetry by modulating the balance between motile and immotile (sensory) cilia at the left-right organiser (LRO).

PTMs:

Synthesized in the endoplasmic reticulum as an inactive form which is proteolytically cleaved by a furin-like convertase in the trans-Golgi network before it reaches the plasma membrane to yield an active, ligand-accessible form (By similarity). Cleavage results in a C-terminal fragment N(TM) and a N-terminal fragment N(EC). Following ligand binding, it is cleaved by ADAM17 to yield a membrane-associated intermediate fragment called notch extracellular truncation (NEXT). Following endocytosis, this fragment is then cleaved by one of the catalytic subunits of gamma-secretase (PSEN1 or PSEN2), to release a Notch-derived peptide containing the intracellular domain (NICD) from the membrane.

Phosphorylated.

O-glycosylated on the EGF-like domains. O-glucosylated at Ser-435 by KDELC1 and KDELC2. Contains both O-linked fucose and O-linked glucose in the EGF-like domains 11, 12 and 13, which are interacting with the residues on DLL4 (By similarity). O-linked glycosylation by GALNT11 is involved in determination of left/right symmetry: glycosylation promotes activation of NOTCH1, possibly by promoting cleavage by ADAM17, modulating the balance between motile and immotile (sensory) cilia at the left-right organiser (LRO). MFNG-, RFNG- and LFNG-mediated modification of O-fucose residues at specific EGF-like domains results in inhibition of its activation by JAG1 and enhancement of its activation by DLL1 via an increased binding to DLL1 (By similarity).

Ubiquitinated. Undergoes 'Lys-29'-linked polyubiquitination by ITCH; promotes the lysosomal degradation of non-activated internalized NOTCH1. Monoubiquitination at Lys-1759 is required for activation by gamma-secretase cleavage, it promotes interaction with AAK1, which stabilizes it. Deubiquitination by EIF3F is necessary for nuclear import of activated Notch.

Hydroxylated at Asn-1955 by HIF1AN. Hydroxylated at Asn-2022 by HIF1AN (By similarity). Hydroxylation reduces affinity for HI1AN and may thus indirectly modulate negative regulation of NICD (By similarity).

Subcellular Location:

Cell membrane>Single-pass type I membrane protein.

Nucleus.
Note: Following proteolytical processing NICD is translocated to the nucleus. Nuclear location may require MEGF10.

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

In fetal tissues most abundant in spleen, brain stem and lung. Also present in most adult tissues where it is found mainly in lymphoid tissues.

Subunit Structure:

Heterodimer of a C-terminal fragment N(TM) and an N-terminal fragment N(EC) which are probably linked by disulfide bonds. Interacts with DNER, DTX1, DTX2 and RBPJ/RBPSUH. Also interacts with MAML1, MAML2 and MAML3 which act as transcriptional coactivators for NOTCH1. The NOTCH1 intracellular domain interacts with SNW1; the interaction involves multimerized NOTCH1 NICD and is implicated in a formation of an intermediate preactivation complex which associates with DNA-bound CBF-1/RBPJ. The activated membrane-bound form interacts with AAK1 which promotes NOTCH1 stabilization. Forms a trimeric complex with FBXW7 and SGK1. Interacts with HIF1AN. HIF1AN negatively regulates the function of notch intracellular domain (NICD), accelerating myogenic differentiation. Interacts (via NICD) with SNAI1 (via zinc fingers); the interaction induces SNAI1 degradation via MDM2-mediated ubiquitination and inhibits SNAI1-induced cell invasion. Interacts (via NICD) with MDM2A. Interacts (via NICD) with BCL6; the interaction decreases MAML1 recruitment by NOTCH1 NICD on target genes DNA and inhibits NOTCH1 transcractivation activity. Interacts with THBS4 (By similarity). Interacts (via the EGF-like repeat region) with CCN3 (via CTCK domain). Interacts (via EGF-like domains) with DLL4 (via N-terminal DSL and MNNL domains) (By similarity). Interacts with ZMIZ1. Interacts (via NICD domain) with MEGF10 (via the cytoplasmic domain). Interacts with DLL1 and JAG1 (By similarity). Interacts (via NICD domain) with PRAG1 (By similarity). Forms a complex with PRAG1, N1ICD and MAML1, in a MAML1-dependent manner (By similarity). Interacts (via transmembrane region) with PSEN1; the interaction is direct.

Family&Domains:

Interaction with PSEN1 causes partial unwinding of the transmembrane helix, facilitating access to the scissile peptide bond.

Belongs to the NOTCH family.

Research Fields

· Environmental Information Processing > Signal transduction > Notch signaling pathway.   (View pathway)

· Human Diseases > Drug resistance: Antineoplastic > Endocrine resistance.

· Human Diseases > Neurodegenerative diseases > Prion diseases.

· Human Diseases > Infectious diseases: Viral > Human papillomavirus infection.

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

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

· Human Diseases > Cancers: Specific types > Breast cancer.   (View pathway)

· Organismal Systems > Immune system > Th1 and Th2 cell differentiation.   (View pathway)

· Organismal Systems > Endocrine system > Thyroid hormone signaling pathway.   (View pathway)

References

1). Organoid modelling identifies that DACH1 functions as a tumour promoter in colorectal cancer by modulating BMP signalling. eBioMedicine (PubMed: 32512510) [IF=11.1]

Application: WB    Species: Human    Sample: HCT116 cells

Fig. 5. DACH1 promotes adenomas organoid formation via modulating BMP signalling. a DACH1 overexpression induced upregulation of cancer stem cell marker genes. b and c. Gene Ontology (GO) analysis showed that DACH1 overexpression induced the upregulation of stem cell signature genes and the downregulation of cell cycle arrest signature genes. d and e. DACH1 induced the downregulation of ATOH8, TGFb3, MSX1, NBL1, BMP7, and FKBP4 and the upregulation of FKBP8, ID1, and MAPK3 (experiments were performed in triplicate). f. IF images showing the colocalization of SMAD4 and DACH1 in the nuclei; scale bars=20 mm g-h. DACH1 coprecipitated endogenous SMAD4. Reverse immunoprecipitation was confirmed with an antiSMAD4 antibody. i. DACH1 overexpression increased the protein level of SMAD4 and decreased the level of phosphorylated SMAD4 (Thr276) [Thr277]. j and k. DACH1 knockdown led to an increase of the mRNA levels of NBL1 and BMP7 compared with the shNC group, and siRNA mediated SMAD4 knockdown in HCT116-shDACH1 cells eliminated the increase. l. DACH1 overexpression was sufficient to compensate for the withdrawal of Noggin and supported the formation of adenoma organoids. m. Addition of Noggin into the culture medium for 24 and 36 h decreased the mRNA levels of NBL1 and BMP7, which were increased by DACH1 knockdown in HCT116 cells. n and o. Overexpression of DACH1 upregulates LGR5, Notch1 and the protein level of NICD, while did not induce significant upregulation of HES1. Scale bars=20 mm. For 5d, 5e, 5k, 5 m and 5n, **P < 0.01, *P < 0.05, Student’s t-test. Error bars: mean§SD.

2). MiR-153 reduces stem cell-like phenotype and tumor growth of lung adenocarcinoma by targeting Jagged1. Stem Cell Research & Therapy (PubMed: 32375892) [IF=7.5]

3). Overexpression of CD59 inhibits apoptosis of T-acute lymphoblastic leukemia via AKT/Notch1 signaling pathway. Cancer Cell International (PubMed: 30636930) [IF=5.8]

Application: WB    Species: human    Sample: Jurkat cells

Fig.?4?|The activation of AKT, STAT5 and Notch1 signaling pathway are involve in the regulation of apoptosis by CD59 in Jurkat cells. The expression of CD59 (a), apoptosis-related proteins (c) and key proteins in signaling pathways (e) detected by western blot. Quantitative analysis of the protein expression of CD59 (b), apoptosis-related proteins (d) and key proteins in signaling pathways (f, g). All experiments were performed three times. *P?

4). Notch1 contributes to TNF-α-induced proliferation and migration of airway smooth muscle cells through regulation of the Hes1/PTEN axis. International Immunopharmacology (PubMed: 32871474) [IF=5.6]

Application: WB    Species: mouse    Sample: ASM cells

Fig. 5.| Notch1 knockdown decreased Hes1 and increased PTEN expression in TNF-α-induced ASM cells. ASM cells were transfected with NC or Notch1 siRNA for 48 h and then stimulated with TNF-α for 24 h. (A, B) Protein expression of NICD was determined by western blot.

5). Lemur tyrosine kinase 2 has a tumor-inhibition function in human glioblastoma by regulating the RUNX3/Notch pathway. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research (PubMed: 37271222) [IF=5.1]

6). Medical Prospect of Melatonin in the Intervertebral Disc Degeneration through Inhibiting M1-Type Macrophage Polarization via SIRT1/Notch Signaling Pathway. Biomedicines (PubMed: 37371708) [IF=4.7]

Application: WB    Species: Mouse    Sample: RAW 264.7 Mφs

Figure 5 Regulation of SIRT1/Notch signal pathway contributes to the effect of MLT on inhibiting M1-type Mφ polarization. RAW 264.7 Mφs were exposed to LPS for 6 h and followed by MLT treatment for 24 h, then treated with SIRT1 agonists (SRT1720) or inhibitors (EX527) for another 6 h and followed by different analysis. (A) Reduction of the ratio of M1-type Mφs while enhancement of the ratio of M2-type Mφs after the treatment with MLT, aggravated in combination with SRT1720, and reversed in the presence of EX527, was determined by flow cytometry assay. (B) The relative mRNA levels of M1-type Mφ genes (IL-6 and TNF-α) and M2-type Mφ genes (IL-4 and IL-10) were measured by RT-qPCR analyses (n = 3). The levels of IL-6 and TNF-α mRNA were reduced in the presence of MLT treatment, downregulated in combination with SRT1720, and upregulated in the presence of EX527. (C,D) The relative protein levels of SIRT1 and NICD in Mφs were measured by Western blot analyses (n = 3). (C) Western blotting showed the upregulation of the SIRT1 protein with the downregulation of the NICD protein, aggravated in combination with SRT1720, and reversed in the presence of EX527. (D) Quantitative analysis showed the increased level of the SIRT1 protein, with the reduced level of the NICD protein after the treatment with MLT, aggravated in combination with SRT1720, and reversed in the presence of EX527. (E) IP with the anti-NICD antibody was used to verify the interaction between SIRT1 and NICD. The interaction between SIRT1 and NICD in the LPS + MLT-treated Mφs was markedly increased compared with that in the LPS-treated Mφs. Moreover, treatment with SRT1720 further aggravated this interaction, while treatment with EX527 ameliorated the interaction. (F) The relative mRNA levels of downstream target genes of the SIRT1/Notch signaling pathway were measured by RT-qPCR analyses in Mφs (n = 3). The levels of Notch1, HES1, HEY2 and NRARP mRNA were downregulated after the treatment with MLT, downregulated in combination with SRT1720, and upregulated in the presence of EX527. (G,H) The relative protein levels of downstream factors of the SIRT1/Notch signaling pathway were measured by Western blot analyses in Mφs (n = 3). (G) Western blotting showed the downregulation of downstream factors protein of the SIRT1/Notch signaling pathway in Mφs. (H) Quantitative analysis showed the reduced levels of Notch1, HES1, HEY2 and NRARP protein after the treatment with MLT, downregulated in combination with SRT1720, and upregulated in the presence of EX527. Data are expressed as mean ± standard deviation. The two groups among the five groups are compared by using an independent t-test.

7). Indoxyl sulfate promotes the atherosclerosis through up-regulating the miR-34a expression in endothelial cells and vascular smooth muscle cells in vitro. VASCULAR PHARMACOLOGY (PubMed: 32593718) [IF=4.0]

Application: WB    Species: human    Sample: HUVECs and HA-VSMCs

Fig. 7.| IS inhibits the Notch signaling pathway and miR-34a-related protein. After transfection with miR-34a mimics (50 nM) or inhibitor (100 nM), IS (1000 μM) was added and incubated for another 36 h. Western blotting was used to detected the protein expression in HUVECs and HA-VSMCs. Data are represented as the mean ± SEM (n = 3). ⁎P < .05, versus control, #P < .05, versus IS group by one-way ANOVA with Tukey's test

8). Notch activity mediates oestrogen-induced stromal cell invasion in endometriosis. REPRODUCTION (PubMed: 30753135) [IF=3.8]

9). Ombuin ameliorates diabetic nephropathy in rats by anti‐inflammation and antifibrosis involving Notch 1 and PPAR γ signaling pathways. DRUG DEVELOPMENT RESEARCH (PubMed: 35672933) [IF=3.8]

10). Notch1/Hes1‑PTEN/AKT/IL‑17A feedback loop regulates Th17 cell differentiation in mouse psoriasis‑like skin inflammation. Molecular Medicine Reports (PubMed: 35582997) [IF=3.4]

Application: WB    Species: mouse    Sample: skin

Figure 6. - Protein levels of (A) Notch1, (B) NICD1, (C) hairy and enhancer of split 1, (D) PTEN, (E-1) p-AKT (Thr308), (E-2) AKT, (E-3) p-AKT (Ser473), (F-1) p-mTOR (Ser2448), (F-2) mTORC1, (G) S6K1 (p70S6Kα), (H) S6K2 (p70S6Kβ) and (I) IL-17A in skin samples of experimental mice. *P

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