human gas6 protein Search Results


gas6 standard  (R&D Systems)
95
R&D Systems gas6 standard
Figure 1. Differentiation of THP-1 cells induced by PMA. (A) THP-1 monocytes are differentiated to macrophages and induced to express Mertk by the addition of 100 ng/mL of PMA for at least 24 h, while Axl expression is not induced. Likewise, Tyro3 expression remains stable and is unaffected by treatment. H1299 and Beas2B cells are used as positive controls for Mertk/Axl and Tyro3, respec- tively. The observed doublet for Mertk corresponds to fully glycosylated and partially glycosylated glycoforms. (B) THP-1 cells treated with 100 ng/mL of PMA over 48 h exhibit a decreased expression of <t>Gas6</t> but an increased expression of Protein S. (C) MertK and Gas6 expression patterns over a time of 48 h after 100 ng/mL of PMA treatment as quantified from Western blots. (D) Bar plots showing MerTK and Gas6 expression quantified from Western blots at 0 h and post 72 h of 100 ng/mL of PMA treatment (significant differences were observed between the 0 h and 72 h time points for Gas6 (* p = 0.029) and MerTK (** p = 0.003), as determined by independent t-tests). (E) THP-1 cells were treated with 100 ng/mL of PMA over 72 h. mRNA was analyzed via qRT-PCR for Mertk, Axl, Protein S (ProS), Tyro3, and Gas6. Mertk transcription was highly elevated, more than 10-fold, due to PMA treatment, while Gas6 transcription was repressed more than 10-fold. (F) PMA treatment of THP-1s illustrates a complimentary phenomenon. As a monocyte, Gas6 is expressed with little Mertk expression; however, when differentiated, Mertk is highly expressed in favor of Gas6.
Gas6 Standard, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human gas6 elisa kit  (Shanghai Korain Biotech Co Ltd)
93
Shanghai Korain Biotech Co Ltd human gas6 elisa kit
Figure 1. Differentiation of THP-1 cells induced by PMA. (A) THP-1 monocytes are differentiated to macrophages and induced to express Mertk by the addition of 100 ng/mL of PMA for at least 24 h, while Axl expression is not induced. Likewise, Tyro3 expression remains stable and is unaffected by treatment. H1299 and Beas2B cells are used as positive controls for Mertk/Axl and Tyro3, respec- tively. The observed doublet for Mertk corresponds to fully glycosylated and partially glycosylated glycoforms. (B) THP-1 cells treated with 100 ng/mL of PMA over 48 h exhibit a decreased expression of <t>Gas6</t> but an increased expression of Protein S. (C) MertK and Gas6 expression patterns over a time of 48 h after 100 ng/mL of PMA treatment as quantified from Western blots. (D) Bar plots showing MerTK and Gas6 expression quantified from Western blots at 0 h and post 72 h of 100 ng/mL of PMA treatment (significant differences were observed between the 0 h and 72 h time points for Gas6 (* p = 0.029) and MerTK (** p = 0.003), as determined by independent t-tests). (E) THP-1 cells were treated with 100 ng/mL of PMA over 72 h. mRNA was analyzed via qRT-PCR for Mertk, Axl, Protein S (ProS), Tyro3, and Gas6. Mertk transcription was highly elevated, more than 10-fold, due to PMA treatment, while Gas6 transcription was repressed more than 10-fold. (F) PMA treatment of THP-1s illustrates a complimentary phenomenon. As a monocyte, Gas6 is expressed with little Mertk expression; however, when differentiated, Mertk is highly expressed in favor of Gas6.
Human Gas6 Elisa Kit, supplied by Shanghai Korain Biotech Co Ltd, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/human gas6 elisa kit/product/Shanghai Korain Biotech Co Ltd
Average 93 stars, based on 1 article reviews
human gas6 elisa kit - by Bioz Stars, 2026-03
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recombinant human gas6  (R&D Systems)
94
R&D Systems recombinant human gas6
Figure 1. Differentiation of THP-1 cells induced by PMA. (A) THP-1 monocytes are differentiated to macrophages and induced to express Mertk by the addition of 100 ng/mL of PMA for at least 24 h, while Axl expression is not induced. Likewise, Tyro3 expression remains stable and is unaffected by treatment. H1299 and Beas2B cells are used as positive controls for Mertk/Axl and Tyro3, respec- tively. The observed doublet for Mertk corresponds to fully glycosylated and partially glycosylated glycoforms. (B) THP-1 cells treated with 100 ng/mL of PMA over 48 h exhibit a decreased expression of <t>Gas6</t> but an increased expression of Protein S. (C) MertK and Gas6 expression patterns over a time of 48 h after 100 ng/mL of PMA treatment as quantified from Western blots. (D) Bar plots showing MerTK and Gas6 expression quantified from Western blots at 0 h and post 72 h of 100 ng/mL of PMA treatment (significant differences were observed between the 0 h and 72 h time points for Gas6 (* p = 0.029) and MerTK (** p = 0.003), as determined by independent t-tests). (E) THP-1 cells were treated with 100 ng/mL of PMA over 72 h. mRNA was analyzed via qRT-PCR for Mertk, Axl, Protein S (ProS), Tyro3, and Gas6. Mertk transcription was highly elevated, more than 10-fold, due to PMA treatment, while Gas6 transcription was repressed more than 10-fold. (F) PMA treatment of THP-1s illustrates a complimentary phenomenon. As a monocyte, Gas6 is expressed with little Mertk expression; however, when differentiated, Mertk is highly expressed in favor of Gas6.
Recombinant Human Gas6, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/recombinant human gas6/product/R&D Systems
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recombinant human gas6 sino biological  (Sino Biological)
90
Sino Biological recombinant human gas6 sino biological
Figure 1. Differentiation of THP-1 cells induced by PMA. (A) THP-1 monocytes are differentiated to macrophages and induced to express Mertk by the addition of 100 ng/mL of PMA for at least 24 h, while Axl expression is not induced. Likewise, Tyro3 expression remains stable and is unaffected by treatment. H1299 and Beas2B cells are used as positive controls for Mertk/Axl and Tyro3, respec- tively. The observed doublet for Mertk corresponds to fully glycosylated and partially glycosylated glycoforms. (B) THP-1 cells treated with 100 ng/mL of PMA over 48 h exhibit a decreased expression of <t>Gas6</t> but an increased expression of Protein S. (C) MertK and Gas6 expression patterns over a time of 48 h after 100 ng/mL of PMA treatment as quantified from Western blots. (D) Bar plots showing MerTK and Gas6 expression quantified from Western blots at 0 h and post 72 h of 100 ng/mL of PMA treatment (significant differences were observed between the 0 h and 72 h time points for Gas6 (* p = 0.029) and MerTK (** p = 0.003), as determined by independent t-tests). (E) THP-1 cells were treated with 100 ng/mL of PMA over 72 h. mRNA was analyzed via qRT-PCR for Mertk, Axl, Protein S (ProS), Tyro3, and Gas6. Mertk transcription was highly elevated, more than 10-fold, due to PMA treatment, while Gas6 transcription was repressed more than 10-fold. (F) PMA treatment of THP-1s illustrates a complimentary phenomenon. As a monocyte, Gas6 is expressed with little Mertk expression; however, when differentiated, Mertk is highly expressed in favor of Gas6.
Recombinant Human Gas6 Sino Biological, supplied by Sino Biological, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/recombinant human gas6 sino biological/product/Sino Biological
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mix gas6  (MedChemExpress)
93
MedChemExpress mix gas6
(A) Binding of different antibodies to AXL. Binding of different antibodies to AXL and their interaction with <t>Gas6.</t> (B) List of full length and different truncations of AXL. (C) αAXL-9# and αAXL-13# were analyzed via flow cytometry for reactivity towards hAXL or hAXL truncations. (D) αAXL-4# were analyzed via flow cytometry for reactivity towards hAXL or hAXL truncations with or without Gas6-his.
Mix Gas6, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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gas6 c01w  (Novoprotein)
90
Novoprotein gas6 c01w
(A) Binding of different antibodies to AXL. Binding of different antibodies to AXL and their interaction with <t>Gas6.</t> (B) List of full length and different truncations of AXL. (C) αAXL-9# and αAXL-13# were analyzed via flow cytometry for reactivity towards hAXL or hAXL truncations. (D) αAXL-4# were analyzed via flow cytometry for reactivity towards hAXL or hAXL truncations with or without Gas6-his.
Gas6 C01w, supplied by Novoprotein, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human gas6 elisa kit  (Boster Bio)
92
Boster Bio human gas6 elisa kit
(A) Binding of different antibodies to AXL. Binding of different antibodies to AXL and their interaction with <t>Gas6.</t> (B) List of full length and different truncations of AXL. (C) αAXL-9# and αAXL-13# were analyzed via flow cytometry for reactivity towards hAXL or hAXL truncations. (D) αAXL-4# were analyzed via flow cytometry for reactivity towards hAXL or hAXL truncations with or without Gas6-his.
Human Gas6 Elisa Kit, supplied by Boster Bio, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/human gas6 elisa kit/product/Boster Bio
Average 92 stars, based on 1 article reviews
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Image Search Results


Figure 1. Differentiation of THP-1 cells induced by PMA. (A) THP-1 monocytes are differentiated to macrophages and induced to express Mertk by the addition of 100 ng/mL of PMA for at least 24 h, while Axl expression is not induced. Likewise, Tyro3 expression remains stable and is unaffected by treatment. H1299 and Beas2B cells are used as positive controls for Mertk/Axl and Tyro3, respec- tively. The observed doublet for Mertk corresponds to fully glycosylated and partially glycosylated glycoforms. (B) THP-1 cells treated with 100 ng/mL of PMA over 48 h exhibit a decreased expression of Gas6 but an increased expression of Protein S. (C) MertK and Gas6 expression patterns over a time of 48 h after 100 ng/mL of PMA treatment as quantified from Western blots. (D) Bar plots showing MerTK and Gas6 expression quantified from Western blots at 0 h and post 72 h of 100 ng/mL of PMA treatment (significant differences were observed between the 0 h and 72 h time points for Gas6 (* p = 0.029) and MerTK (** p = 0.003), as determined by independent t-tests). (E) THP-1 cells were treated with 100 ng/mL of PMA over 72 h. mRNA was analyzed via qRT-PCR for Mertk, Axl, Protein S (ProS), Tyro3, and Gas6. Mertk transcription was highly elevated, more than 10-fold, due to PMA treatment, while Gas6 transcription was repressed more than 10-fold. (F) PMA treatment of THP-1s illustrates a complimentary phenomenon. As a monocyte, Gas6 is expressed with little Mertk expression; however, when differentiated, Mertk is highly expressed in favor of Gas6.

Journal: International journal of molecular sciences

Article Title: Regulation of Mertk Surface Expression via ADAM17 and γ-Secretase Proteolytic Processing.

doi: 10.3390/ijms25084404

Figure Lengend Snippet: Figure 1. Differentiation of THP-1 cells induced by PMA. (A) THP-1 monocytes are differentiated to macrophages and induced to express Mertk by the addition of 100 ng/mL of PMA for at least 24 h, while Axl expression is not induced. Likewise, Tyro3 expression remains stable and is unaffected by treatment. H1299 and Beas2B cells are used as positive controls for Mertk/Axl and Tyro3, respec- tively. The observed doublet for Mertk corresponds to fully glycosylated and partially glycosylated glycoforms. (B) THP-1 cells treated with 100 ng/mL of PMA over 48 h exhibit a decreased expression of Gas6 but an increased expression of Protein S. (C) MertK and Gas6 expression patterns over a time of 48 h after 100 ng/mL of PMA treatment as quantified from Western blots. (D) Bar plots showing MerTK and Gas6 expression quantified from Western blots at 0 h and post 72 h of 100 ng/mL of PMA treatment (significant differences were observed between the 0 h and 72 h time points for Gas6 (* p = 0.029) and MerTK (** p = 0.003), as determined by independent t-tests). (E) THP-1 cells were treated with 100 ng/mL of PMA over 72 h. mRNA was analyzed via qRT-PCR for Mertk, Axl, Protein S (ProS), Tyro3, and Gas6. Mertk transcription was highly elevated, more than 10-fold, due to PMA treatment, while Gas6 transcription was repressed more than 10-fold. (F) PMA treatment of THP-1s illustrates a complimentary phenomenon. As a monocyte, Gas6 is expressed with little Mertk expression; however, when differentiated, Mertk is highly expressed in favor of Gas6.

Article Snippet: Concentrated Gas6 reagents were analyzed for concentration via Western blotting using a Gas6 standard (R&D Systems, 885-GSB-050).

Techniques: Expressing, Western Blot, Quantitative RT-PCR

Figure 3. γ-carboxylated Gas6 Reduces Full-length Mertk Expression and Decreases sMertk. (A) γ- carboxylation status (Gla) of Gas6 is regulated with the addition of Vitamin K or warfarin, producing either a γ-carboxylated, active ligand or a non-γ-carboxylated, inactive ligand, respectively. The carboxylation status (Gla) domain of Gas6 can bind with externalized PS. (B) Recombinant inactive (Gas6-W) and active (Gas6-VK) were produced via HEK293 transfection, with a mock transfection control (Mock). The amount of Gas6 was observed (bottom), while the carboxylation status that is responsible for ligand activity was determined for each (left, top). (C) PMA-differentiated THP-1s were treated for 4 h with either serum-free RPMI only (-), a mock transfection control, 10 nM of active Gas6 (Gas6-VK), or 10 nM of inactive Gas6 (Gas6-W). Treatments were alone or combined with inhibitors of 3 µM of GW280264X (an ADAM17 inhibitor), 5 µM of DAPT (a γ-secretase inhibitor), or 10 µM of MG132 (a proteasomal inhibitor). (D) Quantitative results indicate that Gas6, either active or inactive, does not stabilize the C-terminal fragments as shown in the DAPT and MG132 treatments (bands at 75 kDa). As denoted by sMertk (top), the cleavage is decreased with GW280264X treatment compared to the untreated control.

Journal: International journal of molecular sciences

Article Title: Regulation of Mertk Surface Expression via ADAM17 and γ-Secretase Proteolytic Processing.

doi: 10.3390/ijms25084404

Figure Lengend Snippet: Figure 3. γ-carboxylated Gas6 Reduces Full-length Mertk Expression and Decreases sMertk. (A) γ- carboxylation status (Gla) of Gas6 is regulated with the addition of Vitamin K or warfarin, producing either a γ-carboxylated, active ligand or a non-γ-carboxylated, inactive ligand, respectively. The carboxylation status (Gla) domain of Gas6 can bind with externalized PS. (B) Recombinant inactive (Gas6-W) and active (Gas6-VK) were produced via HEK293 transfection, with a mock transfection control (Mock). The amount of Gas6 was observed (bottom), while the carboxylation status that is responsible for ligand activity was determined for each (left, top). (C) PMA-differentiated THP-1s were treated for 4 h with either serum-free RPMI only (-), a mock transfection control, 10 nM of active Gas6 (Gas6-VK), or 10 nM of inactive Gas6 (Gas6-W). Treatments were alone or combined with inhibitors of 3 µM of GW280264X (an ADAM17 inhibitor), 5 µM of DAPT (a γ-secretase inhibitor), or 10 µM of MG132 (a proteasomal inhibitor). (D) Quantitative results indicate that Gas6, either active or inactive, does not stabilize the C-terminal fragments as shown in the DAPT and MG132 treatments (bands at 75 kDa). As denoted by sMertk (top), the cleavage is decreased with GW280264X treatment compared to the untreated control.

Article Snippet: Concentrated Gas6 reagents were analyzed for concentration via Western blotting using a Gas6 standard (R&D Systems, 885-GSB-050).

Techniques: Expressing, Recombinant, Produced, Transfection, Control, Activity Assay

Figure 5. γ-carboxylated Gas6 reduces the tagged Mertk construct on cell membranes of THP-1 cells. (A) THP-1s expressing the tagged construct were starved for 18 h in serum-free RPMI and treated for 3 h. Flow cytometry data shows positive GFPs without staining. As expected, CHX treatment after 3 h reduces the expression of the construct. Gas6-VK, used at a concentration > 10 nM, decreases the FLAG-PE signal more when compared to other treatments known to induce cleavage (PMA, LPS). GW280264X is used as a control for Mertk cleavage. (B) Histogram analysis of “A.” Gas6-VK induces a shift in the FLAG-PE signal, showing that less surface Mertk is present. γ-Carboxylated Gas6 induced the degradation of Mertk on the cell membrane. (C) THP-1s treated with γ-Carboxylated Gas6 at a 10 nM concentration show increased MerTK phosphorylation, detected by immunoblotting against pMerTK. (D) THP-1s expressing the tagged construct, treated with >10 nM of Gas6-VK + 1 µM of PS, show a reduced level of both domains of the tagged construct, suggesting that the Gas6-VK + PS treatment is leading to a degradation of the full-length receptor.

Journal: International journal of molecular sciences

Article Title: Regulation of Mertk Surface Expression via ADAM17 and γ-Secretase Proteolytic Processing.

doi: 10.3390/ijms25084404

Figure Lengend Snippet: Figure 5. γ-carboxylated Gas6 reduces the tagged Mertk construct on cell membranes of THP-1 cells. (A) THP-1s expressing the tagged construct were starved for 18 h in serum-free RPMI and treated for 3 h. Flow cytometry data shows positive GFPs without staining. As expected, CHX treatment after 3 h reduces the expression of the construct. Gas6-VK, used at a concentration > 10 nM, decreases the FLAG-PE signal more when compared to other treatments known to induce cleavage (PMA, LPS). GW280264X is used as a control for Mertk cleavage. (B) Histogram analysis of “A.” Gas6-VK induces a shift in the FLAG-PE signal, showing that less surface Mertk is present. γ-Carboxylated Gas6 induced the degradation of Mertk on the cell membrane. (C) THP-1s treated with γ-Carboxylated Gas6 at a 10 nM concentration show increased MerTK phosphorylation, detected by immunoblotting against pMerTK. (D) THP-1s expressing the tagged construct, treated with >10 nM of Gas6-VK + 1 µM of PS, show a reduced level of both domains of the tagged construct, suggesting that the Gas6-VK + PS treatment is leading to a degradation of the full-length receptor.

Article Snippet: Concentrated Gas6 reagents were analyzed for concentration via Western blotting using a Gas6 standard (R&D Systems, 885-GSB-050).

Techniques: Construct, Expressing, Flow Cytometry, Staining, Concentration Assay, Control, Membrane, Phospho-proteomics, Western Blot

Figure 6. Confocal imaging of the GFP-tagged MerTK construct displayed the differential localization of MerTK upon ligand stimulation and the inhibition of proteases. (A) DAPT and MG132 treatments induce increased cytoplasmic GFP signals compared to untreated cells. (B) Confocal imaging shows GFP localized on the cell membrane, indicating the presence of tagged Mertk constructs on the cell surface. γ-Carboxylated Gas6-treated tagged THP-1 cells showed a reduction in the MerTK construct from the membrane and the localization in lysosomes. (C) Quantification of the GFP fluorescence intensity per cell, calculated from confocal images in mock, γ-carboxylated Gas6, and non-γ-carboxylated Gas6, with the bar plots showing the mean and standard error of each treatment. ns; non-significant; *** p < 0.001; **** p < 0.0001.

Journal: International journal of molecular sciences

Article Title: Regulation of Mertk Surface Expression via ADAM17 and γ-Secretase Proteolytic Processing.

doi: 10.3390/ijms25084404

Figure Lengend Snippet: Figure 6. Confocal imaging of the GFP-tagged MerTK construct displayed the differential localization of MerTK upon ligand stimulation and the inhibition of proteases. (A) DAPT and MG132 treatments induce increased cytoplasmic GFP signals compared to untreated cells. (B) Confocal imaging shows GFP localized on the cell membrane, indicating the presence of tagged Mertk constructs on the cell surface. γ-Carboxylated Gas6-treated tagged THP-1 cells showed a reduction in the MerTK construct from the membrane and the localization in lysosomes. (C) Quantification of the GFP fluorescence intensity per cell, calculated from confocal images in mock, γ-carboxylated Gas6, and non-γ-carboxylated Gas6, with the bar plots showing the mean and standard error of each treatment. ns; non-significant; *** p < 0.001; **** p < 0.0001.

Article Snippet: Concentrated Gas6 reagents were analyzed for concentration via Western blotting using a Gas6 standard (R&D Systems, 885-GSB-050).

Techniques: Imaging, Construct, Inhibition, Membrane, Fluorescence

Figure 7. γ-carboxylation of Gas6 induces Mertk degradation independent of phosphorylation. (A) Mutants of the tagged construct were created. K619M, a substitution in the ATP-binding site (underlined) of the Mertk kinase domain, inhibits autophosphorylation by preventing ATP binding and the exchange of phosphate molecules. * Amino acid position for ADAM17 cleavage. (B) Constructs are treated with 10 nM ofGas6-VK for 30 min after a 6 h serum starvation. With the ability to bind ATP and phosphorylate, the WT construct becomes phosphorylated while the kinase dead K619M mutant does not. (C) Mutant constructs were treated with 3 µM of GW280264X (an ADAM17 inhibitor; GW), 5 µM of DAPT (a γ-secretase inhibitor), or 10 µM of MG132 (a protea- somal inhibitor) for 4 h. Results show that the absence of the K619M C-terminal fragment from the MG132 treatment with the addition of GW indicates the fragment is a product of cleavage. (D) Confocal images indicated that the K619M mutants have more cytoplasmatic c-Mertk than WT Mertk with MG132 treatment. (E) Comparison of the contrasting pathways between Notch Recep- tor and MerTK Signaling Models. In the absence of a ligand, Notch is not cleaved, while MerTK undergoes homeostatic cleavage, leading to proteasomal degradation. Upon ligand binding, Notch is cleaved at the ADAM 17 site, revealing the gamma-secretase site. Subsequent gamma-secretase cleavage releases the Notch intracellular domain, translocating it to the nucleus for transcriptional activation. Conversely, MerTK, upon ligand (Gas6) interaction, is internalized into endosomal compartments and localizes within lysosomes.

Journal: International journal of molecular sciences

Article Title: Regulation of Mertk Surface Expression via ADAM17 and γ-Secretase Proteolytic Processing.

doi: 10.3390/ijms25084404

Figure Lengend Snippet: Figure 7. γ-carboxylation of Gas6 induces Mertk degradation independent of phosphorylation. (A) Mutants of the tagged construct were created. K619M, a substitution in the ATP-binding site (underlined) of the Mertk kinase domain, inhibits autophosphorylation by preventing ATP binding and the exchange of phosphate molecules. * Amino acid position for ADAM17 cleavage. (B) Constructs are treated with 10 nM ofGas6-VK for 30 min after a 6 h serum starvation. With the ability to bind ATP and phosphorylate, the WT construct becomes phosphorylated while the kinase dead K619M mutant does not. (C) Mutant constructs were treated with 3 µM of GW280264X (an ADAM17 inhibitor; GW), 5 µM of DAPT (a γ-secretase inhibitor), or 10 µM of MG132 (a protea- somal inhibitor) for 4 h. Results show that the absence of the K619M C-terminal fragment from the MG132 treatment with the addition of GW indicates the fragment is a product of cleavage. (D) Confocal images indicated that the K619M mutants have more cytoplasmatic c-Mertk than WT Mertk with MG132 treatment. (E) Comparison of the contrasting pathways between Notch Recep- tor and MerTK Signaling Models. In the absence of a ligand, Notch is not cleaved, while MerTK undergoes homeostatic cleavage, leading to proteasomal degradation. Upon ligand binding, Notch is cleaved at the ADAM 17 site, revealing the gamma-secretase site. Subsequent gamma-secretase cleavage releases the Notch intracellular domain, translocating it to the nucleus for transcriptional activation. Conversely, MerTK, upon ligand (Gas6) interaction, is internalized into endosomal compartments and localizes within lysosomes.

Article Snippet: Concentrated Gas6 reagents were analyzed for concentration via Western blotting using a Gas6 standard (R&D Systems, 885-GSB-050).

Techniques: Phospho-proteomics, Construct, Binding Assay, Mutagenesis, Comparison, Ligand Binding Assay, Activation Assay

(A) Binding of different antibodies to AXL. Binding of different antibodies to AXL and their interaction with Gas6. (B) List of full length and different truncations of AXL. (C) αAXL-9# and αAXL-13# were analyzed via flow cytometry for reactivity towards hAXL or hAXL truncations. (D) αAXL-4# were analyzed via flow cytometry for reactivity towards hAXL or hAXL truncations with or without Gas6-his.

Journal: Frontiers in Medicine

Article Title: Detection of Gas6/AXL complex and its expression changes in patients with ST-segment elevation myocardial infarction

doi: 10.3389/fmed.2025.1653708

Figure Lengend Snippet: (A) Binding of different antibodies to AXL. Binding of different antibodies to AXL and their interaction with Gas6. (B) List of full length and different truncations of AXL. (C) αAXL-9# and αAXL-13# were analyzed via flow cytometry for reactivity towards hAXL or hAXL truncations. (D) αAXL-4# were analyzed via flow cytometry for reactivity towards hAXL or hAXL truncations with or without Gas6-his.

Article Snippet: As previously reported , mix Gas6 (250 ng/mL, HY- P70470 , MCE) with AXL (30 ng/mL, DY154, R&D Systems) in a total volume at 20 μL for 1 h to obtain the AXL-Gas6 complex.

Techniques: Binding Assay, Flow Cytometry

The binding characteristic of AXL-4#. (A) Representation of interplay of AXL antibody and Gas6. (B) 293T-hAXL cells were incubated with isotype control (left), AXL-4# (middle) or AXL4# with Gas6 (right), then stained with PE-goat anti mice IgG2a. (C) 293T-memGas6 cells were incubated with anti-Gas6l (left), AXL-4# (middle) or AXL4# with Gas6 (right), then stained with PE-goat anti mice IgG2a. (D,E) The structure of αAXL-4# recognizing Gas6/AXL complex predicted by AlphaFold.

Journal: Frontiers in Medicine

Article Title: Detection of Gas6/AXL complex and its expression changes in patients with ST-segment elevation myocardial infarction

doi: 10.3389/fmed.2025.1653708

Figure Lengend Snippet: The binding characteristic of AXL-4#. (A) Representation of interplay of AXL antibody and Gas6. (B) 293T-hAXL cells were incubated with isotype control (left), AXL-4# (middle) or AXL4# with Gas6 (right), then stained with PE-goat anti mice IgG2a. (C) 293T-memGas6 cells were incubated with anti-Gas6l (left), AXL-4# (middle) or AXL4# with Gas6 (right), then stained with PE-goat anti mice IgG2a. (D,E) The structure of αAXL-4# recognizing Gas6/AXL complex predicted by AlphaFold.

Article Snippet: As previously reported , mix Gas6 (250 ng/mL, HY- P70470 , MCE) with AXL (30 ng/mL, DY154, R&D Systems) in a total volume at 20 μL for 1 h to obtain the AXL-Gas6 complex.

Techniques: Binding Assay, Incubation, Control, Staining

Application of αAXL-4# in flow cytometry. (A,B) The binding of αAXL-4# to Gas6/AXL complex of different Species. (C,D) asDCs and other cell lines were incubated with αAXL-9#, αAXL-13 and αAXL-4#.

Journal: Frontiers in Medicine

Article Title: Detection of Gas6/AXL complex and its expression changes in patients with ST-segment elevation myocardial infarction

doi: 10.3389/fmed.2025.1653708

Figure Lengend Snippet: Application of αAXL-4# in flow cytometry. (A,B) The binding of αAXL-4# to Gas6/AXL complex of different Species. (C,D) asDCs and other cell lines were incubated with αAXL-9#, αAXL-13 and αAXL-4#.

Article Snippet: As previously reported , mix Gas6 (250 ng/mL, HY- P70470 , MCE) with AXL (30 ng/mL, DY154, R&D Systems) in a total volume at 20 μL for 1 h to obtain the AXL-Gas6 complex.

Techniques: Flow Cytometry, Binding Assay, Incubation

Application of αAXL-4# in ELISA. (A) Different concentrations of AXL (0-1 μg/mL) with a single dose of Gas6 (0.25 μg/mL, red column) or without Gas6 (empty column) were added subsequently. (B) Different concentrations of Gas6 (0–1 μg/mL) with a single dose of AXL (1 μg/mL, red column) or without AXL (empty column) were added subsequently.

Journal: Frontiers in Medicine

Article Title: Detection of Gas6/AXL complex and its expression changes in patients with ST-segment elevation myocardial infarction

doi: 10.3389/fmed.2025.1653708

Figure Lengend Snippet: Application of αAXL-4# in ELISA. (A) Different concentrations of AXL (0-1 μg/mL) with a single dose of Gas6 (0.25 μg/mL, red column) or without Gas6 (empty column) were added subsequently. (B) Different concentrations of Gas6 (0–1 μg/mL) with a single dose of AXL (1 μg/mL, red column) or without AXL (empty column) were added subsequently.

Article Snippet: As previously reported , mix Gas6 (250 ng/mL, HY- P70470 , MCE) with AXL (30 ng/mL, DY154, R&D Systems) in a total volume at 20 μL for 1 h to obtain the AXL-Gas6 complex.

Techniques: Enzyme-linked Immunosorbent Assay

Different levels of AXL-Gas6, AXL and Gas6 in human plasma. (A–C) Plates were coated by AXL-4# (A) , commercial AXL antibody (B) or commercial Gas6 antibody (C) respectively. The levels of AXL-Gas6, AXL, or Gas6 in human plasma were detected by ELISA.

Journal: Frontiers in Medicine

Article Title: Detection of Gas6/AXL complex and its expression changes in patients with ST-segment elevation myocardial infarction

doi: 10.3389/fmed.2025.1653708

Figure Lengend Snippet: Different levels of AXL-Gas6, AXL and Gas6 in human plasma. (A–C) Plates were coated by AXL-4# (A) , commercial AXL antibody (B) or commercial Gas6 antibody (C) respectively. The levels of AXL-Gas6, AXL, or Gas6 in human plasma were detected by ELISA.

Article Snippet: As previously reported , mix Gas6 (250 ng/mL, HY- P70470 , MCE) with AXL (30 ng/mL, DY154, R&D Systems) in a total volume at 20 μL for 1 h to obtain the AXL-Gas6 complex.

Techniques: Clinical Proteomics, Enzyme-linked Immunosorbent Assay

ROC curve and association with AXL/AXL-Gas6 with clinical data. (A) ROC curve; (B) AXL was associated with Cr in STEMI; (C–G) Gas6/AXL complex was associated with PLT, WBC, HDL, CK-MB and SO-FMC as indicated.

Journal: Frontiers in Medicine

Article Title: Detection of Gas6/AXL complex and its expression changes in patients with ST-segment elevation myocardial infarction

doi: 10.3389/fmed.2025.1653708

Figure Lengend Snippet: ROC curve and association with AXL/AXL-Gas6 with clinical data. (A) ROC curve; (B) AXL was associated with Cr in STEMI; (C–G) Gas6/AXL complex was associated with PLT, WBC, HDL, CK-MB and SO-FMC as indicated.

Article Snippet: As previously reported , mix Gas6 (250 ng/mL, HY- P70470 , MCE) with AXL (30 ng/mL, DY154, R&D Systems) in a total volume at 20 μL for 1 h to obtain the AXL-Gas6 complex.

Techniques: