keratinocyte growth Search Results


keratinocyte growth kit  (ATCC)
96
ATCC keratinocyte growth kit
Hematoxylin and eosin (H&E) staining of skin biopsy samples from mice (that allowed feeding of mock/ XM_002400035 -dsRNA-treated ticks) display that tick feeding causes inflammation at bite site in mock-dsRNA-treated group ( A ), but inflammation is reduced in XM_002400035 -dsRNA-treated group ( B ). Within the panniculus, there is downward projection of epidermis containing chitinous tick mouthparts (shown by black arrow). The panniculus contained moderate to large number of neutrophils, lymphocytes, plasma cells, and lower number of macrophages in mice that allowed feeding of mock-dsRNA-treated ticks ( A ). However, panniculus contained moderate number of inflammatory cells (shown by black arrow) with lymphocytes mixed with few macrophages and plasma cells in mice that allowed feeding of XM_002400035 -dsRNA-treated ticks. There is a mild crush artifact in this image. Magnification of both these images is 200×. Scale bar indicates 100 μm for each image. Enlarged images shown in Fig. 9A,B are repeated in Appendix Fig. for better visualization. ( C ) ELISA assay performed with skin lysates from mice that allowed feeding of ticks silenced for exosomal GRP or mock control ticks. Samples were probed with serum from immunized mice (1:1000 dilution). ( D ) Scratch assays performed on HaCaT cell monolayers incubated with 2 µg of GST/GST- GRP/GST-CXCL-12 protein (for 12 h), with/without 20 µl of tick exosomes from uninfected (UI), LGTV-infected (I), LGTV-infected and mock-dsRNA-treated or LGTV-infected and XM_002400035 -dsRNA-treated groups are shown. Phase contrast images (obtained using EVOS auto-fluorescence system, M7000) of HaCaT cell monolayers were taken for selected time-points (as before scratch, 0, 16, 20, and 24 h) and using 10× magnification. Untreated (UT) monolayers served as internal control. Scale bar indicates 275 μm for each image per group or timepoint. ( E ) Measurement of remaining wound size diameters (analyzed by ImageJ software) at different time-points (of 0, 16, 20, and 24 h) post-treatment of tick exosomes-derived from UI, I, mock/ XM_002400035 -dsRNA is shown. Wounds at 0 h were considered as 100% for all groups, including untreated (UT) control. Mouse CXCL-12 expression was analyzed in skin samples from mice immunized with GST/GST-GRP protein is shown ( F ). Exact number of sample numbers for each group representing multiple experiments is 5 mice for GST/6 mice for GST-GRP groups (in C , F ). Statistical differences were calculated using Mann–Whitney U test and p value is shown. p < 0.05 is considered as statistically significant. ( G ) Schematic model showing tick-borne flavivirus transmission to vertebrate host via tick saliva-derived exosomes. Ixodes scapularis tick attaches firmly and bites on host skin for longer feeding. Secreted saliva contains a plethora of substances including cement and perhaps cement-like GRPs to seal the feeding cone/cavity for directional blood flow and to defend from being groomed off by the vertebrate host. During blood meal ingestion, infected-ticks may continuously spit saliva containing infectious exosomes with viral full-length RNA genomes or polyproteins at host skin interface. We propose that incubation of tick exosomes containing exosomal GRP modulates the battle ground at skin interface by delaying cell migration/recruitment of immune cells (like neutrophils and dendritic cells from circulation) at the wound/bite site. Tick exosomes containing GRP inhibits residential <t>keratinocytes</t> and IL-8/CXCL-12 to delay injury, wound-healing, tissue damage, and repair process that will eventually enable ticks to acquire a successful blood meal at the host skin interface. .
Keratinocyte Growth Kit, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/keratinocyte+growth/pmc12993085-38-0-4?v=ATCC
Average 96 stars, based on 1 article reviews
keratinocyte growth kit - by Bioz Stars, 2026-07
96/100 stars
  Buy from Supplier
fgf7  (Gold Biotechnology Inc)
90
Gold Biotechnology Inc fgf7
Hematoxylin and eosin (H&E) staining of skin biopsy samples from mice (that allowed feeding of mock/ XM_002400035 -dsRNA-treated ticks) display that tick feeding causes inflammation at bite site in mock-dsRNA-treated group ( A ), but inflammation is reduced in XM_002400035 -dsRNA-treated group ( B ). Within the panniculus, there is downward projection of epidermis containing chitinous tick mouthparts (shown by black arrow). The panniculus contained moderate to large number of neutrophils, lymphocytes, plasma cells, and lower number of macrophages in mice that allowed feeding of mock-dsRNA-treated ticks ( A ). However, panniculus contained moderate number of inflammatory cells (shown by black arrow) with lymphocytes mixed with few macrophages and plasma cells in mice that allowed feeding of XM_002400035 -dsRNA-treated ticks. There is a mild crush artifact in this image. Magnification of both these images is 200×. Scale bar indicates 100 μm for each image. Enlarged images shown in Fig. 9A,B are repeated in Appendix Fig. for better visualization. ( C ) ELISA assay performed with skin lysates from mice that allowed feeding of ticks silenced for exosomal GRP or mock control ticks. Samples were probed with serum from immunized mice (1:1000 dilution). ( D ) Scratch assays performed on HaCaT cell monolayers incubated with 2 µg of GST/GST- GRP/GST-CXCL-12 protein (for 12 h), with/without 20 µl of tick exosomes from uninfected (UI), LGTV-infected (I), LGTV-infected and mock-dsRNA-treated or LGTV-infected and XM_002400035 -dsRNA-treated groups are shown. Phase contrast images (obtained using EVOS auto-fluorescence system, M7000) of HaCaT cell monolayers were taken for selected time-points (as before scratch, 0, 16, 20, and 24 h) and using 10× magnification. Untreated (UT) monolayers served as internal control. Scale bar indicates 275 μm for each image per group or timepoint. ( E ) Measurement of remaining wound size diameters (analyzed by ImageJ software) at different time-points (of 0, 16, 20, and 24 h) post-treatment of tick exosomes-derived from UI, I, mock/ XM_002400035 -dsRNA is shown. Wounds at 0 h were considered as 100% for all groups, including untreated (UT) control. Mouse CXCL-12 expression was analyzed in skin samples from mice immunized with GST/GST-GRP protein is shown ( F ). Exact number of sample numbers for each group representing multiple experiments is 5 mice for GST/6 mice for GST-GRP groups (in C , F ). Statistical differences were calculated using Mann–Whitney U test and p value is shown. p < 0.05 is considered as statistically significant. ( G ) Schematic model showing tick-borne flavivirus transmission to vertebrate host via tick saliva-derived exosomes. Ixodes scapularis tick attaches firmly and bites on host skin for longer feeding. Secreted saliva contains a plethora of substances including cement and perhaps cement-like GRPs to seal the feeding cone/cavity for directional blood flow and to defend from being groomed off by the vertebrate host. During blood meal ingestion, infected-ticks may continuously spit saliva containing infectious exosomes with viral full-length RNA genomes or polyproteins at host skin interface. We propose that incubation of tick exosomes containing exosomal GRP modulates the battle ground at skin interface by delaying cell migration/recruitment of immune cells (like neutrophils and dendritic cells from circulation) at the wound/bite site. Tick exosomes containing GRP inhibits residential <t>keratinocytes</t> and IL-8/CXCL-12 to delay injury, wound-healing, tissue damage, and repair process that will eventually enable ticks to acquire a successful blood meal at the host skin interface. .
Fgf7, supplied by Gold Biotechnology Inc, 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/product/keratinocyte+growth/pmc07131950-61-48-52?v=Gold+Biotechnology+Inc
Average 90 stars, based on 1 article reviews
fgf7 - by Bioz Stars, 2026-07
90/100 stars
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mouse sil 7rα elisa kits  (Rockland Immunochemicals)
91
Rockland Immunochemicals mouse sil 7rα elisa kits
Hematoxylin and eosin (H&E) staining of skin biopsy samples from mice (that allowed feeding of mock/ XM_002400035 -dsRNA-treated ticks) display that tick feeding causes inflammation at bite site in mock-dsRNA-treated group ( A ), but inflammation is reduced in XM_002400035 -dsRNA-treated group ( B ). Within the panniculus, there is downward projection of epidermis containing chitinous tick mouthparts (shown by black arrow). The panniculus contained moderate to large number of neutrophils, lymphocytes, plasma cells, and lower number of macrophages in mice that allowed feeding of mock-dsRNA-treated ticks ( A ). However, panniculus contained moderate number of inflammatory cells (shown by black arrow) with lymphocytes mixed with few macrophages and plasma cells in mice that allowed feeding of XM_002400035 -dsRNA-treated ticks. There is a mild crush artifact in this image. Magnification of both these images is 200×. Scale bar indicates 100 μm for each image. Enlarged images shown in Fig. 9A,B are repeated in Appendix Fig. for better visualization. ( C ) ELISA assay performed with skin lysates from mice that allowed feeding of ticks silenced for exosomal GRP or mock control ticks. Samples were probed with serum from immunized mice (1:1000 dilution). ( D ) Scratch assays performed on HaCaT cell monolayers incubated with 2 µg of GST/GST- GRP/GST-CXCL-12 protein (for 12 h), with/without 20 µl of tick exosomes from uninfected (UI), LGTV-infected (I), LGTV-infected and mock-dsRNA-treated or LGTV-infected and XM_002400035 -dsRNA-treated groups are shown. Phase contrast images (obtained using EVOS auto-fluorescence system, M7000) of HaCaT cell monolayers were taken for selected time-points (as before scratch, 0, 16, 20, and 24 h) and using 10× magnification. Untreated (UT) monolayers served as internal control. Scale bar indicates 275 μm for each image per group or timepoint. ( E ) Measurement of remaining wound size diameters (analyzed by ImageJ software) at different time-points (of 0, 16, 20, and 24 h) post-treatment of tick exosomes-derived from UI, I, mock/ XM_002400035 -dsRNA is shown. Wounds at 0 h were considered as 100% for all groups, including untreated (UT) control. Mouse CXCL-12 expression was analyzed in skin samples from mice immunized with GST/GST-GRP protein is shown ( F ). Exact number of sample numbers for each group representing multiple experiments is 5 mice for GST/6 mice for GST-GRP groups (in C , F ). Statistical differences were calculated using Mann–Whitney U test and p value is shown. p < 0.05 is considered as statistically significant. ( G ) Schematic model showing tick-borne flavivirus transmission to vertebrate host via tick saliva-derived exosomes. Ixodes scapularis tick attaches firmly and bites on host skin for longer feeding. Secreted saliva contains a plethora of substances including cement and perhaps cement-like GRPs to seal the feeding cone/cavity for directional blood flow and to defend from being groomed off by the vertebrate host. During blood meal ingestion, infected-ticks may continuously spit saliva containing infectious exosomes with viral full-length RNA genomes or polyproteins at host skin interface. We propose that incubation of tick exosomes containing exosomal GRP modulates the battle ground at skin interface by delaying cell migration/recruitment of immune cells (like neutrophils and dendritic cells from circulation) at the wound/bite site. Tick exosomes containing GRP inhibits residential <t>keratinocytes</t> and IL-8/CXCL-12 to delay injury, wound-healing, tissue damage, and repair process that will eventually enable ticks to acquire a successful blood meal at the host skin interface. .
Mouse Sil 7rα Elisa Kits, supplied by Rockland Immunochemicals, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/keratinocyte+growth/pmc07784671-32-32-36?v=Rockland+Immunochemicals
Average 91 stars, based on 1 article reviews
mouse sil 7rα elisa kits - by Bioz Stars, 2026-07
91/100 stars
  Buy from Supplier
polyclonal rabbit antibody  (Rockland Immunochemicals)
85
Rockland Immunochemicals polyclonal rabbit antibody
Hematoxylin and eosin (H&E) staining of skin biopsy samples from mice (that allowed feeding of mock/ XM_002400035 -dsRNA-treated ticks) display that tick feeding causes inflammation at bite site in mock-dsRNA-treated group ( A ), but inflammation is reduced in XM_002400035 -dsRNA-treated group ( B ). Within the panniculus, there is downward projection of epidermis containing chitinous tick mouthparts (shown by black arrow). The panniculus contained moderate to large number of neutrophils, lymphocytes, plasma cells, and lower number of macrophages in mice that allowed feeding of mock-dsRNA-treated ticks ( A ). However, panniculus contained moderate number of inflammatory cells (shown by black arrow) with lymphocytes mixed with few macrophages and plasma cells in mice that allowed feeding of XM_002400035 -dsRNA-treated ticks. There is a mild crush artifact in this image. Magnification of both these images is 200×. Scale bar indicates 100 μm for each image. Enlarged images shown in Fig. 9A,B are repeated in Appendix Fig. for better visualization. ( C ) ELISA assay performed with skin lysates from mice that allowed feeding of ticks silenced for exosomal GRP or mock control ticks. Samples were probed with serum from immunized mice (1:1000 dilution). ( D ) Scratch assays performed on HaCaT cell monolayers incubated with 2 µg of GST/GST- GRP/GST-CXCL-12 protein (for 12 h), with/without 20 µl of tick exosomes from uninfected (UI), LGTV-infected (I), LGTV-infected and mock-dsRNA-treated or LGTV-infected and XM_002400035 -dsRNA-treated groups are shown. Phase contrast images (obtained using EVOS auto-fluorescence system, M7000) of HaCaT cell monolayers were taken for selected time-points (as before scratch, 0, 16, 20, and 24 h) and using 10× magnification. Untreated (UT) monolayers served as internal control. Scale bar indicates 275 μm for each image per group or timepoint. ( E ) Measurement of remaining wound size diameters (analyzed by ImageJ software) at different time-points (of 0, 16, 20, and 24 h) post-treatment of tick exosomes-derived from UI, I, mock/ XM_002400035 -dsRNA is shown. Wounds at 0 h were considered as 100% for all groups, including untreated (UT) control. Mouse CXCL-12 expression was analyzed in skin samples from mice immunized with GST/GST-GRP protein is shown ( F ). Exact number of sample numbers for each group representing multiple experiments is 5 mice for GST/6 mice for GST-GRP groups (in C , F ). Statistical differences were calculated using Mann–Whitney U test and p value is shown. p < 0.05 is considered as statistically significant. ( G ) Schematic model showing tick-borne flavivirus transmission to vertebrate host via tick saliva-derived exosomes. Ixodes scapularis tick attaches firmly and bites on host skin for longer feeding. Secreted saliva contains a plethora of substances including cement and perhaps cement-like GRPs to seal the feeding cone/cavity for directional blood flow and to defend from being groomed off by the vertebrate host. During blood meal ingestion, infected-ticks may continuously spit saliva containing infectious exosomes with viral full-length RNA genomes or polyproteins at host skin interface. We propose that incubation of tick exosomes containing exosomal GRP modulates the battle ground at skin interface by delaying cell migration/recruitment of immune cells (like neutrophils and dendritic cells from circulation) at the wound/bite site. Tick exosomes containing GRP inhibits residential <t>keratinocytes</t> and IL-8/CXCL-12 to delay injury, wound-healing, tissue damage, and repair process that will eventually enable ticks to acquire a successful blood meal at the host skin interface. .
Polyclonal Rabbit Antibody, supplied by Rockland Immunochemicals, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/keratinocyte+growth/pmc02715676-284-0-12?v=Rockland+Immunochemicals
Average 85 stars, based on 1 article reviews
polyclonal rabbit antibody - by Bioz Stars, 2026-07
85/100 stars
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recombinant human keratinocyte growth factor  (Proteintech)
93
Proteintech recombinant human keratinocyte growth factor
Hematoxylin and eosin (H&E) staining of skin biopsy samples from mice (that allowed feeding of mock/ XM_002400035 -dsRNA-treated ticks) display that tick feeding causes inflammation at bite site in mock-dsRNA-treated group ( A ), but inflammation is reduced in XM_002400035 -dsRNA-treated group ( B ). Within the panniculus, there is downward projection of epidermis containing chitinous tick mouthparts (shown by black arrow). The panniculus contained moderate to large number of neutrophils, lymphocytes, plasma cells, and lower number of macrophages in mice that allowed feeding of mock-dsRNA-treated ticks ( A ). However, panniculus contained moderate number of inflammatory cells (shown by black arrow) with lymphocytes mixed with few macrophages and plasma cells in mice that allowed feeding of XM_002400035 -dsRNA-treated ticks. There is a mild crush artifact in this image. Magnification of both these images is 200×. Scale bar indicates 100 μm for each image. Enlarged images shown in Fig. 9A,B are repeated in Appendix Fig. for better visualization. ( C ) ELISA assay performed with skin lysates from mice that allowed feeding of ticks silenced for exosomal GRP or mock control ticks. Samples were probed with serum from immunized mice (1:1000 dilution). ( D ) Scratch assays performed on HaCaT cell monolayers incubated with 2 µg of GST/GST- GRP/GST-CXCL-12 protein (for 12 h), with/without 20 µl of tick exosomes from uninfected (UI), LGTV-infected (I), LGTV-infected and mock-dsRNA-treated or LGTV-infected and XM_002400035 -dsRNA-treated groups are shown. Phase contrast images (obtained using EVOS auto-fluorescence system, M7000) of HaCaT cell monolayers were taken for selected time-points (as before scratch, 0, 16, 20, and 24 h) and using 10× magnification. Untreated (UT) monolayers served as internal control. Scale bar indicates 275 μm for each image per group or timepoint. ( E ) Measurement of remaining wound size diameters (analyzed by ImageJ software) at different time-points (of 0, 16, 20, and 24 h) post-treatment of tick exosomes-derived from UI, I, mock/ XM_002400035 -dsRNA is shown. Wounds at 0 h were considered as 100% for all groups, including untreated (UT) control. Mouse CXCL-12 expression was analyzed in skin samples from mice immunized with GST/GST-GRP protein is shown ( F ). Exact number of sample numbers for each group representing multiple experiments is 5 mice for GST/6 mice for GST-GRP groups (in C , F ). Statistical differences were calculated using Mann–Whitney U test and p value is shown. p < 0.05 is considered as statistically significant. ( G ) Schematic model showing tick-borne flavivirus transmission to vertebrate host via tick saliva-derived exosomes. Ixodes scapularis tick attaches firmly and bites on host skin for longer feeding. Secreted saliva contains a plethora of substances including cement and perhaps cement-like GRPs to seal the feeding cone/cavity for directional blood flow and to defend from being groomed off by the vertebrate host. During blood meal ingestion, infected-ticks may continuously spit saliva containing infectious exosomes with viral full-length RNA genomes or polyproteins at host skin interface. We propose that incubation of tick exosomes containing exosomal GRP modulates the battle ground at skin interface by delaying cell migration/recruitment of immune cells (like neutrophils and dendritic cells from circulation) at the wound/bite site. Tick exosomes containing GRP inhibits residential <t>keratinocytes</t> and IL-8/CXCL-12 to delay injury, wound-healing, tissue damage, and repair process that will eventually enable ticks to acquire a successful blood meal at the host skin interface. .
Recombinant Human Keratinocyte Growth Factor, supplied by Proteintech, 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/product/keratinocyte+growth/pmc02678735-30-0-11?v=Proteintech
Average 93 stars, based on 1 article reviews
recombinant human keratinocyte growth factor - by Bioz Stars, 2026-07
93/100 stars
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mouse keratinocyte growth factor elisa kit  (Cusabio)
91
Cusabio mouse keratinocyte growth factor elisa kit
Hematoxylin and eosin (H&E) staining of skin biopsy samples from mice (that allowed feeding of mock/ XM_002400035 -dsRNA-treated ticks) display that tick feeding causes inflammation at bite site in mock-dsRNA-treated group ( A ), but inflammation is reduced in XM_002400035 -dsRNA-treated group ( B ). Within the panniculus, there is downward projection of epidermis containing chitinous tick mouthparts (shown by black arrow). The panniculus contained moderate to large number of neutrophils, lymphocytes, plasma cells, and lower number of macrophages in mice that allowed feeding of mock-dsRNA-treated ticks ( A ). However, panniculus contained moderate number of inflammatory cells (shown by black arrow) with lymphocytes mixed with few macrophages and plasma cells in mice that allowed feeding of XM_002400035 -dsRNA-treated ticks. There is a mild crush artifact in this image. Magnification of both these images is 200×. Scale bar indicates 100 μm for each image. Enlarged images shown in Fig. 9A,B are repeated in Appendix Fig. for better visualization. ( C ) ELISA assay performed with skin lysates from mice that allowed feeding of ticks silenced for exosomal GRP or mock control ticks. Samples were probed with serum from immunized mice (1:1000 dilution). ( D ) Scratch assays performed on HaCaT cell monolayers incubated with 2 µg of GST/GST- GRP/GST-CXCL-12 protein (for 12 h), with/without 20 µl of tick exosomes from uninfected (UI), LGTV-infected (I), LGTV-infected and mock-dsRNA-treated or LGTV-infected and XM_002400035 -dsRNA-treated groups are shown. Phase contrast images (obtained using EVOS auto-fluorescence system, M7000) of HaCaT cell monolayers were taken for selected time-points (as before scratch, 0, 16, 20, and 24 h) and using 10× magnification. Untreated (UT) monolayers served as internal control. Scale bar indicates 275 μm for each image per group or timepoint. ( E ) Measurement of remaining wound size diameters (analyzed by ImageJ software) at different time-points (of 0, 16, 20, and 24 h) post-treatment of tick exosomes-derived from UI, I, mock/ XM_002400035 -dsRNA is shown. Wounds at 0 h were considered as 100% for all groups, including untreated (UT) control. Mouse CXCL-12 expression was analyzed in skin samples from mice immunized with GST/GST-GRP protein is shown ( F ). Exact number of sample numbers for each group representing multiple experiments is 5 mice for GST/6 mice for GST-GRP groups (in C , F ). Statistical differences were calculated using Mann–Whitney U test and p value is shown. p < 0.05 is considered as statistically significant. ( G ) Schematic model showing tick-borne flavivirus transmission to vertebrate host via tick saliva-derived exosomes. Ixodes scapularis tick attaches firmly and bites on host skin for longer feeding. Secreted saliva contains a plethora of substances including cement and perhaps cement-like GRPs to seal the feeding cone/cavity for directional blood flow and to defend from being groomed off by the vertebrate host. During blood meal ingestion, infected-ticks may continuously spit saliva containing infectious exosomes with viral full-length RNA genomes or polyproteins at host skin interface. We propose that incubation of tick exosomes containing exosomal GRP modulates the battle ground at skin interface by delaying cell migration/recruitment of immune cells (like neutrophils and dendritic cells from circulation) at the wound/bite site. Tick exosomes containing GRP inhibits residential <t>keratinocytes</t> and IL-8/CXCL-12 to delay injury, wound-healing, tissue damage, and repair process that will eventually enable ticks to acquire a successful blood meal at the host skin interface. .
Mouse Keratinocyte Growth Factor Elisa Kit, supplied by Cusabio, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/keratinocyte+growth/ppr0749388-100-0-6?v=Cusabio
Average 91 stars, based on 1 article reviews
mouse keratinocyte growth factor elisa kit - by Bioz Stars, 2026-07
91/100 stars
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keratinocyte growth medium md 0047  (iXCells Biotechnologies)
93
iXCells Biotechnologies keratinocyte growth medium md 0047
Hematoxylin and eosin (H&E) staining of skin biopsy samples from mice (that allowed feeding of mock/ XM_002400035 -dsRNA-treated ticks) display that tick feeding causes inflammation at bite site in mock-dsRNA-treated group ( A ), but inflammation is reduced in XM_002400035 -dsRNA-treated group ( B ). Within the panniculus, there is downward projection of epidermis containing chitinous tick mouthparts (shown by black arrow). The panniculus contained moderate to large number of neutrophils, lymphocytes, plasma cells, and lower number of macrophages in mice that allowed feeding of mock-dsRNA-treated ticks ( A ). However, panniculus contained moderate number of inflammatory cells (shown by black arrow) with lymphocytes mixed with few macrophages and plasma cells in mice that allowed feeding of XM_002400035 -dsRNA-treated ticks. There is a mild crush artifact in this image. Magnification of both these images is 200×. Scale bar indicates 100 μm for each image. Enlarged images shown in Fig. 9A,B are repeated in Appendix Fig. for better visualization. ( C ) ELISA assay performed with skin lysates from mice that allowed feeding of ticks silenced for exosomal GRP or mock control ticks. Samples were probed with serum from immunized mice (1:1000 dilution). ( D ) Scratch assays performed on HaCaT cell monolayers incubated with 2 µg of GST/GST- GRP/GST-CXCL-12 protein (for 12 h), with/without 20 µl of tick exosomes from uninfected (UI), LGTV-infected (I), LGTV-infected and mock-dsRNA-treated or LGTV-infected and XM_002400035 -dsRNA-treated groups are shown. Phase contrast images (obtained using EVOS auto-fluorescence system, M7000) of HaCaT cell monolayers were taken for selected time-points (as before scratch, 0, 16, 20, and 24 h) and using 10× magnification. Untreated (UT) monolayers served as internal control. Scale bar indicates 275 μm for each image per group or timepoint. ( E ) Measurement of remaining wound size diameters (analyzed by ImageJ software) at different time-points (of 0, 16, 20, and 24 h) post-treatment of tick exosomes-derived from UI, I, mock/ XM_002400035 -dsRNA is shown. Wounds at 0 h were considered as 100% for all groups, including untreated (UT) control. Mouse CXCL-12 expression was analyzed in skin samples from mice immunized with GST/GST-GRP protein is shown ( F ). Exact number of sample numbers for each group representing multiple experiments is 5 mice for GST/6 mice for GST-GRP groups (in C , F ). Statistical differences were calculated using Mann–Whitney U test and p value is shown. p < 0.05 is considered as statistically significant. ( G ) Schematic model showing tick-borne flavivirus transmission to vertebrate host via tick saliva-derived exosomes. Ixodes scapularis tick attaches firmly and bites on host skin for longer feeding. Secreted saliva contains a plethora of substances including cement and perhaps cement-like GRPs to seal the feeding cone/cavity for directional blood flow and to defend from being groomed off by the vertebrate host. During blood meal ingestion, infected-ticks may continuously spit saliva containing infectious exosomes with viral full-length RNA genomes or polyproteins at host skin interface. We propose that incubation of tick exosomes containing exosomal GRP modulates the battle ground at skin interface by delaying cell migration/recruitment of immune cells (like neutrophils and dendritic cells from circulation) at the wound/bite site. Tick exosomes containing GRP inhibits residential <t>keratinocytes</t> and IL-8/CXCL-12 to delay injury, wound-healing, tissue damage, and repair process that will eventually enable ticks to acquire a successful blood meal at the host skin interface. .
Keratinocyte Growth Medium Md 0047, supplied by iXCells Biotechnologies, 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/product/keratinocyte+growth/pmc10821797-201-6-12?v=iXCells+Biotechnologies
Average 93 stars, based on 1 article reviews
keratinocyte growth medium md 0047 - by Bioz Stars, 2026-07
93/100 stars
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keratinocyte growth medium  (Lonza)
97
Lonza keratinocyte growth medium
Hematoxylin and eosin (H&E) staining of skin biopsy samples from mice (that allowed feeding of mock/ XM_002400035 -dsRNA-treated ticks) display that tick feeding causes inflammation at bite site in mock-dsRNA-treated group ( A ), but inflammation is reduced in XM_002400035 -dsRNA-treated group ( B ). Within the panniculus, there is downward projection of epidermis containing chitinous tick mouthparts (shown by black arrow). The panniculus contained moderate to large number of neutrophils, lymphocytes, plasma cells, and lower number of macrophages in mice that allowed feeding of mock-dsRNA-treated ticks ( A ). However, panniculus contained moderate number of inflammatory cells (shown by black arrow) with lymphocytes mixed with few macrophages and plasma cells in mice that allowed feeding of XM_002400035 -dsRNA-treated ticks. There is a mild crush artifact in this image. Magnification of both these images is 200×. Scale bar indicates 100 μm for each image. Enlarged images shown in Fig. 9A,B are repeated in Appendix Fig. for better visualization. ( C ) ELISA assay performed with skin lysates from mice that allowed feeding of ticks silenced for exosomal GRP or mock control ticks. Samples were probed with serum from immunized mice (1:1000 dilution). ( D ) Scratch assays performed on HaCaT cell monolayers incubated with 2 µg of GST/GST- GRP/GST-CXCL-12 protein (for 12 h), with/without 20 µl of tick exosomes from uninfected (UI), LGTV-infected (I), LGTV-infected and mock-dsRNA-treated or LGTV-infected and XM_002400035 -dsRNA-treated groups are shown. Phase contrast images (obtained using EVOS auto-fluorescence system, M7000) of HaCaT cell monolayers were taken for selected time-points (as before scratch, 0, 16, 20, and 24 h) and using 10× magnification. Untreated (UT) monolayers served as internal control. Scale bar indicates 275 μm for each image per group or timepoint. ( E ) Measurement of remaining wound size diameters (analyzed by ImageJ software) at different time-points (of 0, 16, 20, and 24 h) post-treatment of tick exosomes-derived from UI, I, mock/ XM_002400035 -dsRNA is shown. Wounds at 0 h were considered as 100% for all groups, including untreated (UT) control. Mouse CXCL-12 expression was analyzed in skin samples from mice immunized with GST/GST-GRP protein is shown ( F ). Exact number of sample numbers for each group representing multiple experiments is 5 mice for GST/6 mice for GST-GRP groups (in C , F ). Statistical differences were calculated using Mann–Whitney U test and p value is shown. p < 0.05 is considered as statistically significant. ( G ) Schematic model showing tick-borne flavivirus transmission to vertebrate host via tick saliva-derived exosomes. Ixodes scapularis tick attaches firmly and bites on host skin for longer feeding. Secreted saliva contains a plethora of substances including cement and perhaps cement-like GRPs to seal the feeding cone/cavity for directional blood flow and to defend from being groomed off by the vertebrate host. During blood meal ingestion, infected-ticks may continuously spit saliva containing infectious exosomes with viral full-length RNA genomes or polyproteins at host skin interface. We propose that incubation of tick exosomes containing exosomal GRP modulates the battle ground at skin interface by delaying cell migration/recruitment of immune cells (like neutrophils and dendritic cells from circulation) at the wound/bite site. Tick exosomes containing GRP inhibits residential <t>keratinocytes</t> and IL-8/CXCL-12 to delay injury, wound-healing, tissue damage, and repair process that will eventually enable ticks to acquire a successful blood meal at the host skin interface. .
Keratinocyte Growth Medium, supplied by Lonza, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/keratinocyte+growth/pmc05102796-141-17-21?v=Lonza
Average 97 stars, based on 1 article reviews
keratinocyte growth medium - by Bioz Stars, 2026-07
97/100 stars
  Buy from Supplier
fgfr2  (Boster Bio)
90
Boster Bio fgfr2
Hematoxylin and eosin (H&E) staining of skin biopsy samples from mice (that allowed feeding of mock/ XM_002400035 -dsRNA-treated ticks) display that tick feeding causes inflammation at bite site in mock-dsRNA-treated group ( A ), but inflammation is reduced in XM_002400035 -dsRNA-treated group ( B ). Within the panniculus, there is downward projection of epidermis containing chitinous tick mouthparts (shown by black arrow). The panniculus contained moderate to large number of neutrophils, lymphocytes, plasma cells, and lower number of macrophages in mice that allowed feeding of mock-dsRNA-treated ticks ( A ). However, panniculus contained moderate number of inflammatory cells (shown by black arrow) with lymphocytes mixed with few macrophages and plasma cells in mice that allowed feeding of XM_002400035 -dsRNA-treated ticks. There is a mild crush artifact in this image. Magnification of both these images is 200×. Scale bar indicates 100 μm for each image. Enlarged images shown in Fig. 9A,B are repeated in Appendix Fig. for better visualization. ( C ) ELISA assay performed with skin lysates from mice that allowed feeding of ticks silenced for exosomal GRP or mock control ticks. Samples were probed with serum from immunized mice (1:1000 dilution). ( D ) Scratch assays performed on HaCaT cell monolayers incubated with 2 µg of GST/GST- GRP/GST-CXCL-12 protein (for 12 h), with/without 20 µl of tick exosomes from uninfected (UI), LGTV-infected (I), LGTV-infected and mock-dsRNA-treated or LGTV-infected and XM_002400035 -dsRNA-treated groups are shown. Phase contrast images (obtained using EVOS auto-fluorescence system, M7000) of HaCaT cell monolayers were taken for selected time-points (as before scratch, 0, 16, 20, and 24 h) and using 10× magnification. Untreated (UT) monolayers served as internal control. Scale bar indicates 275 μm for each image per group or timepoint. ( E ) Measurement of remaining wound size diameters (analyzed by ImageJ software) at different time-points (of 0, 16, 20, and 24 h) post-treatment of tick exosomes-derived from UI, I, mock/ XM_002400035 -dsRNA is shown. Wounds at 0 h were considered as 100% for all groups, including untreated (UT) control. Mouse CXCL-12 expression was analyzed in skin samples from mice immunized with GST/GST-GRP protein is shown ( F ). Exact number of sample numbers for each group representing multiple experiments is 5 mice for GST/6 mice for GST-GRP groups (in C , F ). Statistical differences were calculated using Mann–Whitney U test and p value is shown. p < 0.05 is considered as statistically significant. ( G ) Schematic model showing tick-borne flavivirus transmission to vertebrate host via tick saliva-derived exosomes. Ixodes scapularis tick attaches firmly and bites on host skin for longer feeding. Secreted saliva contains a plethora of substances including cement and perhaps cement-like GRPs to seal the feeding cone/cavity for directional blood flow and to defend from being groomed off by the vertebrate host. During blood meal ingestion, infected-ticks may continuously spit saliva containing infectious exosomes with viral full-length RNA genomes or polyproteins at host skin interface. We propose that incubation of tick exosomes containing exosomal GRP modulates the battle ground at skin interface by delaying cell migration/recruitment of immune cells (like neutrophils and dendritic cells from circulation) at the wound/bite site. Tick exosomes containing GRP inhibits residential <t>keratinocytes</t> and IL-8/CXCL-12 to delay injury, wound-healing, tissue damage, and repair process that will eventually enable ticks to acquire a successful blood meal at the host skin interface. .
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Hematoxylin and eosin (H&E) staining of skin biopsy samples from mice (that allowed feeding of mock/ XM_002400035 -dsRNA-treated ticks) display that tick feeding causes inflammation at bite site in mock-dsRNA-treated group ( A ), but inflammation is reduced in XM_002400035 -dsRNA-treated group ( B ). Within the panniculus, there is downward projection of epidermis containing chitinous tick mouthparts (shown by black arrow). The panniculus contained moderate to large number of neutrophils, lymphocytes, plasma cells, and lower number of macrophages in mice that allowed feeding of mock-dsRNA-treated ticks ( A ). However, panniculus contained moderate number of inflammatory cells (shown by black arrow) with lymphocytes mixed with few macrophages and plasma cells in mice that allowed feeding of XM_002400035 -dsRNA-treated ticks. There is a mild crush artifact in this image. Magnification of both these images is 200×. Scale bar indicates 100 μm for each image. Enlarged images shown in Fig. 9A,B are repeated in Appendix Fig. for better visualization. ( C ) ELISA assay performed with skin lysates from mice that allowed feeding of ticks silenced for exosomal GRP or mock control ticks. Samples were probed with serum from immunized mice (1:1000 dilution). ( D ) Scratch assays performed on HaCaT cell monolayers incubated with 2 µg of GST/GST- GRP/GST-CXCL-12 protein (for 12 h), with/without 20 µl of tick exosomes from uninfected (UI), LGTV-infected (I), LGTV-infected and mock-dsRNA-treated or LGTV-infected and XM_002400035 -dsRNA-treated groups are shown. Phase contrast images (obtained using EVOS auto-fluorescence system, M7000) of HaCaT cell monolayers were taken for selected time-points (as before scratch, 0, 16, 20, and 24 h) and using 10× magnification. Untreated (UT) monolayers served as internal control. Scale bar indicates 275 μm for each image per group or timepoint. ( E ) Measurement of remaining wound size diameters (analyzed by ImageJ software) at different time-points (of 0, 16, 20, and 24 h) post-treatment of tick exosomes-derived from UI, I, mock/ XM_002400035 -dsRNA is shown. Wounds at 0 h were considered as 100% for all groups, including untreated (UT) control. Mouse CXCL-12 expression was analyzed in skin samples from mice immunized with GST/GST-GRP protein is shown ( F ). Exact number of sample numbers for each group representing multiple experiments is 5 mice for GST/6 mice for GST-GRP groups (in C , F ). Statistical differences were calculated using Mann–Whitney U test and p value is shown. p < 0.05 is considered as statistically significant. ( G ) Schematic model showing tick-borne flavivirus transmission to vertebrate host via tick saliva-derived exosomes. Ixodes scapularis tick attaches firmly and bites on host skin for longer feeding. Secreted saliva contains a plethora of substances including cement and perhaps cement-like GRPs to seal the feeding cone/cavity for directional blood flow and to defend from being groomed off by the vertebrate host. During blood meal ingestion, infected-ticks may continuously spit saliva containing infectious exosomes with viral full-length RNA genomes or polyproteins at host skin interface. We propose that incubation of tick exosomes containing exosomal GRP modulates the battle ground at skin interface by delaying cell migration/recruitment of immune cells (like neutrophils and dendritic cells from circulation) at the wound/bite site. Tick exosomes containing GRP inhibits residential <t>keratinocytes</t> and IL-8/CXCL-12 to delay injury, wound-healing, tissue damage, and repair process that will eventually enable ticks to acquire a successful blood meal at the host skin interface. .
Anti Fgf10, supplied by Boster Bio, 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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Hematoxylin and eosin (H&E) staining of skin biopsy samples from mice (that allowed feeding of mock/ XM_002400035 -dsRNA-treated ticks) display that tick feeding causes inflammation at bite site in mock-dsRNA-treated group ( A ), but inflammation is reduced in XM_002400035 -dsRNA-treated group ( B ). Within the panniculus, there is downward projection of epidermis containing chitinous tick mouthparts (shown by black arrow). The panniculus contained moderate to large number of neutrophils, lymphocytes, plasma cells, and lower number of macrophages in mice that allowed feeding of mock-dsRNA-treated ticks ( A ). However, panniculus contained moderate number of inflammatory cells (shown by black arrow) with lymphocytes mixed with few macrophages and plasma cells in mice that allowed feeding of XM_002400035 -dsRNA-treated ticks. There is a mild crush artifact in this image. Magnification of both these images is 200×. Scale bar indicates 100 μm for each image. Enlarged images shown in Fig. 9A,B are repeated in Appendix Fig. for better visualization. ( C ) ELISA assay performed with skin lysates from mice that allowed feeding of ticks silenced for exosomal GRP or mock control ticks. Samples were probed with serum from immunized mice (1:1000 dilution). ( D ) Scratch assays performed on HaCaT cell monolayers incubated with 2 µg of GST/GST- GRP/GST-CXCL-12 protein (for 12 h), with/without 20 µl of tick exosomes from uninfected (UI), LGTV-infected (I), LGTV-infected and mock-dsRNA-treated or LGTV-infected and XM_002400035 -dsRNA-treated groups are shown. Phase contrast images (obtained using EVOS auto-fluorescence system, M7000) of HaCaT cell monolayers were taken for selected time-points (as before scratch, 0, 16, 20, and 24 h) and using 10× magnification. Untreated (UT) monolayers served as internal control. Scale bar indicates 275 μm for each image per group or timepoint. ( E ) Measurement of remaining wound size diameters (analyzed by ImageJ software) at different time-points (of 0, 16, 20, and 24 h) post-treatment of tick exosomes-derived from UI, I, mock/ XM_002400035 -dsRNA is shown. Wounds at 0 h were considered as 100% for all groups, including untreated (UT) control. Mouse CXCL-12 expression was analyzed in skin samples from mice immunized with GST/GST-GRP protein is shown ( F ). Exact number of sample numbers for each group representing multiple experiments is 5 mice for GST/6 mice for GST-GRP groups (in C , F ). Statistical differences were calculated using Mann–Whitney U test and p value is shown. p < 0.05 is considered as statistically significant. ( G ) Schematic model showing tick-borne flavivirus transmission to vertebrate host via tick saliva-derived exosomes. Ixodes scapularis tick attaches firmly and bites on host skin for longer feeding. Secreted saliva contains a plethora of substances including cement and perhaps cement-like GRPs to seal the feeding cone/cavity for directional blood flow and to defend from being groomed off by the vertebrate host. During blood meal ingestion, infected-ticks may continuously spit saliva containing infectious exosomes with viral full-length RNA genomes or polyproteins at host skin interface. We propose that incubation of tick exosomes containing exosomal GRP modulates the battle ground at skin interface by delaying cell migration/recruitment of immune cells (like neutrophils and dendritic cells from circulation) at the wound/bite site. Tick exosomes containing GRP inhibits residential <t>keratinocytes</t> and IL-8/CXCL-12 to delay injury, wound-healing, tissue damage, and repair process that will eventually enable ticks to acquire a successful blood meal at the host skin interface. .
Recombinant Lumen Keratinocyte Growth Factor Kgf, supplied by Chiron Technologies Ltd, 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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Image Search Results


Hematoxylin and eosin (H&E) staining of skin biopsy samples from mice (that allowed feeding of mock/ XM_002400035 -dsRNA-treated ticks) display that tick feeding causes inflammation at bite site in mock-dsRNA-treated group ( A ), but inflammation is reduced in XM_002400035 -dsRNA-treated group ( B ). Within the panniculus, there is downward projection of epidermis containing chitinous tick mouthparts (shown by black arrow). The panniculus contained moderate to large number of neutrophils, lymphocytes, plasma cells, and lower number of macrophages in mice that allowed feeding of mock-dsRNA-treated ticks ( A ). However, panniculus contained moderate number of inflammatory cells (shown by black arrow) with lymphocytes mixed with few macrophages and plasma cells in mice that allowed feeding of XM_002400035 -dsRNA-treated ticks. There is a mild crush artifact in this image. Magnification of both these images is 200×. Scale bar indicates 100 μm for each image. Enlarged images shown in Fig. 9A,B are repeated in Appendix Fig. for better visualization. ( C ) ELISA assay performed with skin lysates from mice that allowed feeding of ticks silenced for exosomal GRP or mock control ticks. Samples were probed with serum from immunized mice (1:1000 dilution). ( D ) Scratch assays performed on HaCaT cell monolayers incubated with 2 µg of GST/GST- GRP/GST-CXCL-12 protein (for 12 h), with/without 20 µl of tick exosomes from uninfected (UI), LGTV-infected (I), LGTV-infected and mock-dsRNA-treated or LGTV-infected and XM_002400035 -dsRNA-treated groups are shown. Phase contrast images (obtained using EVOS auto-fluorescence system, M7000) of HaCaT cell monolayers were taken for selected time-points (as before scratch, 0, 16, 20, and 24 h) and using 10× magnification. Untreated (UT) monolayers served as internal control. Scale bar indicates 275 μm for each image per group or timepoint. ( E ) Measurement of remaining wound size diameters (analyzed by ImageJ software) at different time-points (of 0, 16, 20, and 24 h) post-treatment of tick exosomes-derived from UI, I, mock/ XM_002400035 -dsRNA is shown. Wounds at 0 h were considered as 100% for all groups, including untreated (UT) control. Mouse CXCL-12 expression was analyzed in skin samples from mice immunized with GST/GST-GRP protein is shown ( F ). Exact number of sample numbers for each group representing multiple experiments is 5 mice for GST/6 mice for GST-GRP groups (in C , F ). Statistical differences were calculated using Mann–Whitney U test and p value is shown. p < 0.05 is considered as statistically significant. ( G ) Schematic model showing tick-borne flavivirus transmission to vertebrate host via tick saliva-derived exosomes. Ixodes scapularis tick attaches firmly and bites on host skin for longer feeding. Secreted saliva contains a plethora of substances including cement and perhaps cement-like GRPs to seal the feeding cone/cavity for directional blood flow and to defend from being groomed off by the vertebrate host. During blood meal ingestion, infected-ticks may continuously spit saliva containing infectious exosomes with viral full-length RNA genomes or polyproteins at host skin interface. We propose that incubation of tick exosomes containing exosomal GRP modulates the battle ground at skin interface by delaying cell migration/recruitment of immune cells (like neutrophils and dendritic cells from circulation) at the wound/bite site. Tick exosomes containing GRP inhibits residential keratinocytes and IL-8/CXCL-12 to delay injury, wound-healing, tissue damage, and repair process that will eventually enable ticks to acquire a successful blood meal at the host skin interface. .

Journal: The EMBO Journal

Article Title: Arthropod exosomal glycine-rich protein as a potential vaccine candidate effectively reduces tick blood-feeding and pathogen transmission

doi: 10.1038/s44318-026-00709-z

Figure Lengend Snippet: Hematoxylin and eosin (H&E) staining of skin biopsy samples from mice (that allowed feeding of mock/ XM_002400035 -dsRNA-treated ticks) display that tick feeding causes inflammation at bite site in mock-dsRNA-treated group ( A ), but inflammation is reduced in XM_002400035 -dsRNA-treated group ( B ). Within the panniculus, there is downward projection of epidermis containing chitinous tick mouthparts (shown by black arrow). The panniculus contained moderate to large number of neutrophils, lymphocytes, plasma cells, and lower number of macrophages in mice that allowed feeding of mock-dsRNA-treated ticks ( A ). However, panniculus contained moderate number of inflammatory cells (shown by black arrow) with lymphocytes mixed with few macrophages and plasma cells in mice that allowed feeding of XM_002400035 -dsRNA-treated ticks. There is a mild crush artifact in this image. Magnification of both these images is 200×. Scale bar indicates 100 μm for each image. Enlarged images shown in Fig. 9A,B are repeated in Appendix Fig. for better visualization. ( C ) ELISA assay performed with skin lysates from mice that allowed feeding of ticks silenced for exosomal GRP or mock control ticks. Samples were probed with serum from immunized mice (1:1000 dilution). ( D ) Scratch assays performed on HaCaT cell monolayers incubated with 2 µg of GST/GST- GRP/GST-CXCL-12 protein (for 12 h), with/without 20 µl of tick exosomes from uninfected (UI), LGTV-infected (I), LGTV-infected and mock-dsRNA-treated or LGTV-infected and XM_002400035 -dsRNA-treated groups are shown. Phase contrast images (obtained using EVOS auto-fluorescence system, M7000) of HaCaT cell monolayers were taken for selected time-points (as before scratch, 0, 16, 20, and 24 h) and using 10× magnification. Untreated (UT) monolayers served as internal control. Scale bar indicates 275 μm for each image per group or timepoint. ( E ) Measurement of remaining wound size diameters (analyzed by ImageJ software) at different time-points (of 0, 16, 20, and 24 h) post-treatment of tick exosomes-derived from UI, I, mock/ XM_002400035 -dsRNA is shown. Wounds at 0 h were considered as 100% for all groups, including untreated (UT) control. Mouse CXCL-12 expression was analyzed in skin samples from mice immunized with GST/GST-GRP protein is shown ( F ). Exact number of sample numbers for each group representing multiple experiments is 5 mice for GST/6 mice for GST-GRP groups (in C , F ). Statistical differences were calculated using Mann–Whitney U test and p value is shown. p < 0.05 is considered as statistically significant. ( G ) Schematic model showing tick-borne flavivirus transmission to vertebrate host via tick saliva-derived exosomes. Ixodes scapularis tick attaches firmly and bites on host skin for longer feeding. Secreted saliva contains a plethora of substances including cement and perhaps cement-like GRPs to seal the feeding cone/cavity for directional blood flow and to defend from being groomed off by the vertebrate host. During blood meal ingestion, infected-ticks may continuously spit saliva containing infectious exosomes with viral full-length RNA genomes or polyproteins at host skin interface. We propose that incubation of tick exosomes containing exosomal GRP modulates the battle ground at skin interface by delaying cell migration/recruitment of immune cells (like neutrophils and dendritic cells from circulation) at the wound/bite site. Tick exosomes containing GRP inhibits residential keratinocytes and IL-8/CXCL-12 to delay injury, wound-healing, tissue damage, and repair process that will eventually enable ticks to acquire a successful blood meal at the host skin interface. .

Article Snippet: Keratinocyte growth kit , ATCC , # PCS-200-040.

Techniques: Staining, Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Control, Incubation, Infection, Fluorescence, Software, Derivative Assay, Expressing, MANN-WHITNEY, Transmission Assay, Migration