cell culture medium am 1 Search Results


staining solution  (Dojindo Labs)
97
Dojindo Labs staining solution
Staining Solution, supplied by Dojindo Labs, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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m extorquens am1  (ATCC)
94
ATCC m extorquens am1
M Extorquens Am1, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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adipocyte medium am-1  (ZenBio)
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ZenBio adipocyte medium am-1
Adipocyte Medium Am 1, supplied by ZenBio, 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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3t3-l1 adipocyte medium am-1-l1  (ZenBio)
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ZenBio 3t3-l1 adipocyte medium am-1-l1
3t3 L1 Adipocyte Medium Am 1 L1, supplied by ZenBio, 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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cyclopamine  (Toronto Research Chemicals)
94
Toronto Research Chemicals cyclopamine
Fig. 7. Shh-N mediates RA-dependent dorso-ventral specification of ES-cell-derived neural progenitors. (A) Expression of Shh and its active N-terminal truncated form, Shh-N, in EBs cultured for 6 days, was analyzed by Western blotting. EBs were exposed to various concentrations of RA. Quantitative analysis was performed with Scion Image. The amounts of proteins were normalized to those of a-tubulin (B) (n = 3, mean F SEM, *, P b 0.05 vs. control. y, P b 0.05 vs. RA 2 106 M). (C) RT-PCR analysis of shh and bmp4. Shh-N was more highly expressed in EBs treated with low-RA (109 M–108 M). (D) RT-PCR analysis of RA-exposed EBs treated with Shh-N and its inhibitor <t>cyclopamine.</t> Shh-N and cyclopamine were added together with RA on day 2. (E) Summary of expression patterns in vitro corresponding to in vivo. Cells from low-RA-treated EBs were a mixed population of dorsal-to-ventral neural progenitors and were capable of being dorsalized by inhibiting Shh signaling with cyclopamine. By contrast, exogenous Shh-N induced ventral neural progenitors were capable of being dorsalized by cyclopamine. Cells from high-RA-treated EBs showed dorsal positional identities. However, addition of Shh-N increased the number of ventral neural progenitors, and they were also capable of being dorsalized by cyclopamine treatment.
Cyclopamine, supplied by Toronto Research Chemicals, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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tni 19c7 am1 hg1 cho 204  (ATCC)
95
ATCC tni 19c7 am1 hg1 cho 204
Fig. 7. Shh-N mediates RA-dependent dorso-ventral specification of ES-cell-derived neural progenitors. (A) Expression of Shh and its active N-terminal truncated form, Shh-N, in EBs cultured for 6 days, was analyzed by Western blotting. EBs were exposed to various concentrations of RA. Quantitative analysis was performed with Scion Image. The amounts of proteins were normalized to those of a-tubulin (B) (n = 3, mean F SEM, *, P b 0.05 vs. control. y, P b 0.05 vs. RA 2 106 M). (C) RT-PCR analysis of shh and bmp4. Shh-N was more highly expressed in EBs treated with low-RA (109 M–108 M). (D) RT-PCR analysis of RA-exposed EBs treated with Shh-N and its inhibitor <t>cyclopamine.</t> Shh-N and cyclopamine were added together with RA on day 2. (E) Summary of expression patterns in vitro corresponding to in vivo. Cells from low-RA-treated EBs were a mixed population of dorsal-to-ventral neural progenitors and were capable of being dorsalized by inhibiting Shh signaling with cyclopamine. By contrast, exogenous Shh-N induced ventral neural progenitors were capable of being dorsalized by cyclopamine. Cells from high-RA-treated EBs showed dorsal positional identities. However, addition of Shh-N increased the number of ventral neural progenitors, and they were also capable of being dorsalized by cyclopamine treatment.
Tni 19c7 Am1 Hg1 Cho 204, supplied by ATCC, 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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bacteroides intestinalis am 1 strain dsm 17393  (DSMZ)
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DSMZ bacteroides intestinalis am 1 strain dsm 17393
Fig. 7. Shh-N mediates RA-dependent dorso-ventral specification of ES-cell-derived neural progenitors. (A) Expression of Shh and its active N-terminal truncated form, Shh-N, in EBs cultured for 6 days, was analyzed by Western blotting. EBs were exposed to various concentrations of RA. Quantitative analysis was performed with Scion Image. The amounts of proteins were normalized to those of a-tubulin (B) (n = 3, mean F SEM, *, P b 0.05 vs. control. y, P b 0.05 vs. RA 2 106 M). (C) RT-PCR analysis of shh and bmp4. Shh-N was more highly expressed in EBs treated with low-RA (109 M–108 M). (D) RT-PCR analysis of RA-exposed EBs treated with Shh-N and its inhibitor <t>cyclopamine.</t> Shh-N and cyclopamine were added together with RA on day 2. (E) Summary of expression patterns in vitro corresponding to in vivo. Cells from low-RA-treated EBs were a mixed population of dorsal-to-ventral neural progenitors and were capable of being dorsalized by inhibiting Shh signaling with cyclopamine. By contrast, exogenous Shh-N induced ventral neural progenitors were capable of being dorsalized by cyclopamine. Cells from high-RA-treated EBs showed dorsal positional identities. However, addition of Shh-N increased the number of ventral neural progenitors, and they were also capable of being dorsalized by cyclopamine treatment.
Bacteroides Intestinalis Am 1 Strain Dsm 17393, supplied by DSMZ, 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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mil 38 hybridoma preparations ausmab 1 and 2  (ATCC)
92
ATCC mil 38 hybridoma preparations ausmab 1 and 2
Fig. 7. Shh-N mediates RA-dependent dorso-ventral specification of ES-cell-derived neural progenitors. (A) Expression of Shh and its active N-terminal truncated form, Shh-N, in EBs cultured for 6 days, was analyzed by Western blotting. EBs were exposed to various concentrations of RA. Quantitative analysis was performed with Scion Image. The amounts of proteins were normalized to those of a-tubulin (B) (n = 3, mean F SEM, *, P b 0.05 vs. control. y, P b 0.05 vs. RA 2 106 M). (C) RT-PCR analysis of shh and bmp4. Shh-N was more highly expressed in EBs treated with low-RA (109 M–108 M). (D) RT-PCR analysis of RA-exposed EBs treated with Shh-N and its inhibitor <t>cyclopamine.</t> Shh-N and cyclopamine were added together with RA on day 2. (E) Summary of expression patterns in vitro corresponding to in vivo. Cells from low-RA-treated EBs were a mixed population of dorsal-to-ventral neural progenitors and were capable of being dorsalized by inhibiting Shh signaling with cyclopamine. By contrast, exogenous Shh-N induced ventral neural progenitors were capable of being dorsalized by cyclopamine. Cells from high-RA-treated EBs showed dorsal positional identities. However, addition of Shh-N increased the number of ventral neural progenitors, and they were also capable of being dorsalized by cyclopamine treatment.
Mil 38 Hybridoma Preparations Ausmab 1 And 2, supplied by ATCC, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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am1 1845  (ATCC)
92
ATCC am1 1845
Fig. 7. Shh-N mediates RA-dependent dorso-ventral specification of ES-cell-derived neural progenitors. (A) Expression of Shh and its active N-terminal truncated form, Shh-N, in EBs cultured for 6 days, was analyzed by Western blotting. EBs were exposed to various concentrations of RA. Quantitative analysis was performed with Scion Image. The amounts of proteins were normalized to those of a-tubulin (B) (n = 3, mean F SEM, *, P b 0.05 vs. control. y, P b 0.05 vs. RA 2 106 M). (C) RT-PCR analysis of shh and bmp4. Shh-N was more highly expressed in EBs treated with low-RA (109 M–108 M). (D) RT-PCR analysis of RA-exposed EBs treated with Shh-N and its inhibitor <t>cyclopamine.</t> Shh-N and cyclopamine were added together with RA on day 2. (E) Summary of expression patterns in vitro corresponding to in vivo. Cells from low-RA-treated EBs were a mixed population of dorsal-to-ventral neural progenitors and were capable of being dorsalized by inhibiting Shh signaling with cyclopamine. By contrast, exogenous Shh-N induced ventral neural progenitors were capable of being dorsalized by cyclopamine. Cells from high-RA-treated EBs showed dorsal positional identities. However, addition of Shh-N increased the number of ventral neural progenitors, and they were also capable of being dorsalized by cyclopamine treatment.
Am1 1845, supplied by ATCC, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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rcc307 synrcc307 2198 synrcc307 2197 acaryochloris marina mbic11017 am1 0109 am1 0110 synechococcus sp  (ATCC)
94
ATCC rcc307 synrcc307 2198 synrcc307 2197 acaryochloris marina mbic11017 am1 0109 am1 0110 synechococcus sp
Fig. 7. Shh-N mediates RA-dependent dorso-ventral specification of ES-cell-derived neural progenitors. (A) Expression of Shh and its active N-terminal truncated form, Shh-N, in EBs cultured for 6 days, was analyzed by Western blotting. EBs were exposed to various concentrations of RA. Quantitative analysis was performed with Scion Image. The amounts of proteins were normalized to those of a-tubulin (B) (n = 3, mean F SEM, *, P b 0.05 vs. control. y, P b 0.05 vs. RA 2 106 M). (C) RT-PCR analysis of shh and bmp4. Shh-N was more highly expressed in EBs treated with low-RA (109 M–108 M). (D) RT-PCR analysis of RA-exposed EBs treated with Shh-N and its inhibitor <t>cyclopamine.</t> Shh-N and cyclopamine were added together with RA on day 2. (E) Summary of expression patterns in vitro corresponding to in vivo. Cells from low-RA-treated EBs were a mixed population of dorsal-to-ventral neural progenitors and were capable of being dorsalized by inhibiting Shh signaling with cyclopamine. By contrast, exogenous Shh-N induced ventral neural progenitors were capable of being dorsalized by cyclopamine. Cells from high-RA-treated EBs showed dorsal positional identities. However, addition of Shh-N increased the number of ventral neural progenitors, and they were also capable of being dorsalized by cyclopamine treatment.
Rcc307 Synrcc307 2198 Synrcc307 2197 Acaryochloris Marina Mbic11017 Am1 0109 Am1 0110 Synechococcus Sp, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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am1 h0057 abw33407 gspe  (ATCC)
95
ATCC am1 h0057 abw33407 gspe
Fig. 7. Shh-N mediates RA-dependent dorso-ventral specification of ES-cell-derived neural progenitors. (A) Expression of Shh and its active N-terminal truncated form, Shh-N, in EBs cultured for 6 days, was analyzed by Western blotting. EBs were exposed to various concentrations of RA. Quantitative analysis was performed with Scion Image. The amounts of proteins were normalized to those of a-tubulin (B) (n = 3, mean F SEM, *, P b 0.05 vs. control. y, P b 0.05 vs. RA 2 106 M). (C) RT-PCR analysis of shh and bmp4. Shh-N was more highly expressed in EBs treated with low-RA (109 M–108 M). (D) RT-PCR analysis of RA-exposed EBs treated with Shh-N and its inhibitor <t>cyclopamine.</t> Shh-N and cyclopamine were added together with RA on day 2. (E) Summary of expression patterns in vitro corresponding to in vivo. Cells from low-RA-treated EBs were a mixed population of dorsal-to-ventral neural progenitors and were capable of being dorsalized by inhibiting Shh signaling with cyclopamine. By contrast, exogenous Shh-N induced ventral neural progenitors were capable of being dorsalized by cyclopamine. Cells from high-RA-treated EBs showed dorsal positional identities. However, addition of Shh-N increased the number of ventral neural progenitors, and they were also capable of being dorsalized by cyclopamine treatment.
Am1 H0057 Abw33407 Gspe, supplied by ATCC, 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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am-1-l1 medium  (ZenBio)
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ZenBio am-1-l1 medium
Fig. 7. Shh-N mediates RA-dependent dorso-ventral specification of ES-cell-derived neural progenitors. (A) Expression of Shh and its active N-terminal truncated form, Shh-N, in EBs cultured for 6 days, was analyzed by Western blotting. EBs were exposed to various concentrations of RA. Quantitative analysis was performed with Scion Image. The amounts of proteins were normalized to those of a-tubulin (B) (n = 3, mean F SEM, *, P b 0.05 vs. control. y, P b 0.05 vs. RA 2 106 M). (C) RT-PCR analysis of shh and bmp4. Shh-N was more highly expressed in EBs treated with low-RA (109 M–108 M). (D) RT-PCR analysis of RA-exposed EBs treated with Shh-N and its inhibitor <t>cyclopamine.</t> Shh-N and cyclopamine were added together with RA on day 2. (E) Summary of expression patterns in vitro corresponding to in vivo. Cells from low-RA-treated EBs were a mixed population of dorsal-to-ventral neural progenitors and were capable of being dorsalized by inhibiting Shh signaling with cyclopamine. By contrast, exogenous Shh-N induced ventral neural progenitors were capable of being dorsalized by cyclopamine. Cells from high-RA-treated EBs showed dorsal positional identities. However, addition of Shh-N increased the number of ventral neural progenitors, and they were also capable of being dorsalized by cyclopamine treatment.
Am 1 L1 Medium, supplied by ZenBio, 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


Fig. 7. Shh-N mediates RA-dependent dorso-ventral specification of ES-cell-derived neural progenitors. (A) Expression of Shh and its active N-terminal truncated form, Shh-N, in EBs cultured for 6 days, was analyzed by Western blotting. EBs were exposed to various concentrations of RA. Quantitative analysis was performed with Scion Image. The amounts of proteins were normalized to those of a-tubulin (B) (n = 3, mean F SEM, *, P b 0.05 vs. control. y, P b 0.05 vs. RA 2 106 M). (C) RT-PCR analysis of shh and bmp4. Shh-N was more highly expressed in EBs treated with low-RA (109 M–108 M). (D) RT-PCR analysis of RA-exposed EBs treated with Shh-N and its inhibitor cyclopamine. Shh-N and cyclopamine were added together with RA on day 2. (E) Summary of expression patterns in vitro corresponding to in vivo. Cells from low-RA-treated EBs were a mixed population of dorsal-to-ventral neural progenitors and were capable of being dorsalized by inhibiting Shh signaling with cyclopamine. By contrast, exogenous Shh-N induced ventral neural progenitors were capable of being dorsalized by cyclopamine. Cells from high-RA-treated EBs showed dorsal positional identities. However, addition of Shh-N increased the number of ventral neural progenitors, and they were also capable of being dorsalized by cyclopamine treatment.

Journal: Developmental biology

Article Title: Retinoic-acid-concentration-dependent acquisition of neural cell identity during in vitro differentiation of mouse embryonic stem cells.

doi: 10.1016/j.ydbio.2004.07.038

Figure Lengend Snippet: Fig. 7. Shh-N mediates RA-dependent dorso-ventral specification of ES-cell-derived neural progenitors. (A) Expression of Shh and its active N-terminal truncated form, Shh-N, in EBs cultured for 6 days, was analyzed by Western blotting. EBs were exposed to various concentrations of RA. Quantitative analysis was performed with Scion Image. The amounts of proteins were normalized to those of a-tubulin (B) (n = 3, mean F SEM, *, P b 0.05 vs. control. y, P b 0.05 vs. RA 2 106 M). (C) RT-PCR analysis of shh and bmp4. Shh-N was more highly expressed in EBs treated with low-RA (109 M–108 M). (D) RT-PCR analysis of RA-exposed EBs treated with Shh-N and its inhibitor cyclopamine. Shh-N and cyclopamine were added together with RA on day 2. (E) Summary of expression patterns in vitro corresponding to in vivo. Cells from low-RA-treated EBs were a mixed population of dorsal-to-ventral neural progenitors and were capable of being dorsalized by inhibiting Shh signaling with cyclopamine. By contrast, exogenous Shh-N induced ventral neural progenitors were capable of being dorsalized by cyclopamine. Cells from high-RA-treated EBs showed dorsal positional identities. However, addition of Shh-N increased the number of ventral neural progenitors, and they were also capable of being dorsalized by cyclopamine treatment.

Article Snippet: Recombinant mouse Sonic Hedgehog (Shh) protein (amino-teminal peptide) (Shh-N; R&D Systems Inc., 461-SH) and cyclopamine (0.1 AM, 1 AM, Toronto Research Chemicals Inc., C988400) were also added on day 2 of the experiment.

Techniques: Derivative Assay, Expressing, Cell Culture, Western Blot, Control, Reverse Transcription Polymerase Chain Reaction, In Vitro, In Vivo