unaffected control pcs 201 010 Search Results


pcs 500 010 crl 2522  (ATCC)
95
ATCC pcs 500 010 crl 2522
Pcs 500 010 Crl 2522, 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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il 1β  (R&D Systems)
96
R&D Systems il 1β
Il 1β, supplied by R&D Systems, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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equine fibroblastic cell line  (ATCC)
99
ATCC equine fibroblastic cell line
Equine Fibroblastic Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/unaffected+control+pcs+201+010/Primary+Dermal+Fibroblast+Normal%3B+Human%2C+Neonatal/pmc02258727-153-3-11
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neonatal dermal fibroblasts  (ATCC)
95
ATCC neonatal dermal fibroblasts
Neonatal Dermal Fibroblasts, 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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huvec  (ATCC)
96
ATCC huvec
Huvec, 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
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fibroblast cells  (ATCC)
94
ATCC fibroblast cells
Fibroblast Cells, 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
https://www.bioz.com/product/unaffected+control+pcs+201+010/Primary+Lung+Fibroblasts%3B+Cystic+Fibrosis%2C+Human/us10973775-163-10-12
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human fibroblasts  (ATCC)
93
ATCC human fibroblasts
Human Fibroblasts, supplied by ATCC, 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/unaffected+control+pcs+201+010/Leptographium+pyrinum+Davidson%2C+anamorph/pmc03644353-53-6-13
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human fibroblasts - by Bioz Stars, 2026-09
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primary dermal fibroblasts  (ATCC)
99
ATCC primary dermal fibroblasts
Expression of wild-type (WT) and mutant transcripts in affected family members with the heterozygous c.618+836 T > G growth hormone receptor ( GHR ) 6Ω variant. The GHR 6Ω pseudoexon also diminishes GH-dependent STAT5B activation and accumulates extracellularly. A, Complementary DNA (cDNA) was prepared from dermal <t>fibroblasts</t> derived from a healthy control (HC) and patients 2 (P2) and P3 and both parents. Schematic showing the locations of the primers ( GHR cDNA exon 4F [forward] and GHR cDNA exon 8R [reverse] [blue arrows]) used to amplify the region encompassing WT GHR , the GHR 6Ω pseudoexon insertion. A “normal” 705–base pair (bp) polymerase chain reaction (PCR) product was seen in all samples. An additional larger (856-bp) PCR product was seen in P2, P3, and their mother, who were heterozygous for the c.618+836 T > G GHR 6Ω variant, indicating the additional 151-bp 6Ω pseudoexon insertion. B, Schematic showing the locations of the primers ( GHR cDNA pseudo F1 [forward] and GHR cDNA exon 8R [reverse] [blue arrows]). The forward primer at the junction of the 6Ω pseudoexon insertion means only sequences containing the GHR 6Ω pseudoexon insertion are amplified. The expected 387-bp PCR product is seen in patient 2, patient 3, and their mother, all of whom are heterozygous for the c.618+836 T > G GHR variant. C, Whole-cell lysates from untreated or GH-stimulated (20 minutes) HEK293 cells transfected with pcDNA3.1 empty vector, WT GHR or 6Ω GHR mutant constructs. Representative immunoblots of 3 experiments are shown. D, Immunoblot analysis of conditioned media with anti-GH binding protein (BP) antibody from HEK293 cells transfected with the 6Ω GHR mutant construct showing extracellular accumulation of the truncated mutant 6Ω GHR protein. B actin, β actin; K2M, kindred 2 mother; K2F kindred 2 father.
Primary Dermal Fibroblasts, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/unaffected+control+pcs+201+010/Primary+Dermal+Fibroblast%3B+Normal%2C+Human%2C+Adult/pmc08684449-130-0-8
Average 99 stars, based on 1 article reviews
primary dermal fibroblasts - by Bioz Stars, 2026-09
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uttar pradesh  (Wolters Kluwer Health)
86
Wolters Kluwer Health uttar pradesh
Expression of wild-type (WT) and mutant transcripts in affected family members with the heterozygous c.618+836 T > G growth hormone receptor ( GHR ) 6Ω variant. The GHR 6Ω pseudoexon also diminishes GH-dependent STAT5B activation and accumulates extracellularly. A, Complementary DNA (cDNA) was prepared from dermal <t>fibroblasts</t> derived from a healthy control (HC) and patients 2 (P2) and P3 and both parents. Schematic showing the locations of the primers ( GHR cDNA exon 4F [forward] and GHR cDNA exon 8R [reverse] [blue arrows]) used to amplify the region encompassing WT GHR , the GHR 6Ω pseudoexon insertion. A “normal” 705–base pair (bp) polymerase chain reaction (PCR) product was seen in all samples. An additional larger (856-bp) PCR product was seen in P2, P3, and their mother, who were heterozygous for the c.618+836 T > G GHR 6Ω variant, indicating the additional 151-bp 6Ω pseudoexon insertion. B, Schematic showing the locations of the primers ( GHR cDNA pseudo F1 [forward] and GHR cDNA exon 8R [reverse] [blue arrows]). The forward primer at the junction of the 6Ω pseudoexon insertion means only sequences containing the GHR 6Ω pseudoexon insertion are amplified. The expected 387-bp PCR product is seen in patient 2, patient 3, and their mother, all of whom are heterozygous for the c.618+836 T > G GHR variant. C, Whole-cell lysates from untreated or GH-stimulated (20 minutes) HEK293 cells transfected with pcDNA3.1 empty vector, WT GHR or 6Ω GHR mutant constructs. Representative immunoblots of 3 experiments are shown. D, Immunoblot analysis of conditioned media with anti-GH binding protein (BP) antibody from HEK293 cells transfected with the 6Ω GHR mutant construct showing extracellular accumulation of the truncated mutant 6Ω GHR protein. B actin, β actin; K2M, kindred 2 mother; K2F kindred 2 father.
Uttar Pradesh, supplied by Wolters Kluwer Health, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/unaffected+control+pcs+201+010/pradesh+uttar/10__4103_slash_endo__endo_48_24-9-33-6
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human primary fibroblast culture  (ATCC)
95
ATCC human primary fibroblast culture
Expression of wild-type (WT) and mutant transcripts in affected family members with the heterozygous c.618+836 T > G growth hormone receptor ( GHR ) 6Ω variant. The GHR 6Ω pseudoexon also diminishes GH-dependent STAT5B activation and accumulates extracellularly. A, Complementary DNA (cDNA) was prepared from dermal <t>fibroblasts</t> derived from a healthy control (HC) and patients 2 (P2) and P3 and both parents. Schematic showing the locations of the primers ( GHR cDNA exon 4F [forward] and GHR cDNA exon 8R [reverse] [blue arrows]) used to amplify the region encompassing WT GHR , the GHR 6Ω pseudoexon insertion. A “normal” 705–base pair (bp) polymerase chain reaction (PCR) product was seen in all samples. An additional larger (856-bp) PCR product was seen in P2, P3, and their mother, who were heterozygous for the c.618+836 T > G GHR 6Ω variant, indicating the additional 151-bp 6Ω pseudoexon insertion. B, Schematic showing the locations of the primers ( GHR cDNA pseudo F1 [forward] and GHR cDNA exon 8R [reverse] [blue arrows]). The forward primer at the junction of the 6Ω pseudoexon insertion means only sequences containing the GHR 6Ω pseudoexon insertion are amplified. The expected 387-bp PCR product is seen in patient 2, patient 3, and their mother, all of whom are heterozygous for the c.618+836 T > G GHR variant. C, Whole-cell lysates from untreated or GH-stimulated (20 minutes) HEK293 cells transfected with pcDNA3.1 empty vector, WT GHR or 6Ω GHR mutant constructs. Representative immunoblots of 3 experiments are shown. D, Immunoblot analysis of conditioned media with anti-GH binding protein (BP) antibody from HEK293 cells transfected with the 6Ω GHR mutant construct showing extracellular accumulation of the truncated mutant 6Ω GHR protein. B actin, β actin; K2M, kindred 2 mother; K2F kindred 2 father.
Human Primary Fibroblast Culture, 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
https://www.bioz.com/product/unaffected+control+pcs+201+010/Human+skin+fibroblast/pmc07765732-79-0-11
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fibroblast lines  (ATCC)
95
ATCC fibroblast lines
Expression of wild-type (WT) and mutant transcripts in affected family members with the heterozygous c.618+836 T > G growth hormone receptor ( GHR ) 6Ω variant. The GHR 6Ω pseudoexon also diminishes GH-dependent STAT5B activation and accumulates extracellularly. A, Complementary DNA (cDNA) was prepared from dermal <t>fibroblasts</t> derived from a healthy control (HC) and patients 2 (P2) and P3 and both parents. Schematic showing the locations of the primers ( GHR cDNA exon 4F [forward] and GHR cDNA exon 8R [reverse] [blue arrows]) used to amplify the region encompassing WT GHR , the GHR 6Ω pseudoexon insertion. A “normal” 705–base pair (bp) polymerase chain reaction (PCR) product was seen in all samples. An additional larger (856-bp) PCR product was seen in P2, P3, and their mother, who were heterozygous for the c.618+836 T > G GHR 6Ω variant, indicating the additional 151-bp 6Ω pseudoexon insertion. B, Schematic showing the locations of the primers ( GHR cDNA pseudo F1 [forward] and GHR cDNA exon 8R [reverse] [blue arrows]). The forward primer at the junction of the 6Ω pseudoexon insertion means only sequences containing the GHR 6Ω pseudoexon insertion are amplified. The expected 387-bp PCR product is seen in patient 2, patient 3, and their mother, all of whom are heterozygous for the c.618+836 T > G GHR variant. C, Whole-cell lysates from untreated or GH-stimulated (20 minutes) HEK293 cells transfected with pcDNA3.1 empty vector, WT GHR or 6Ω GHR mutant constructs. Representative immunoblots of 3 experiments are shown. D, Immunoblot analysis of conditioned media with anti-GH binding protein (BP) antibody from HEK293 cells transfected with the 6Ω GHR mutant construct showing extracellular accumulation of the truncated mutant 6Ω GHR protein. B actin, β actin; K2M, kindred 2 mother; K2F kindred 2 father.
Fibroblast Lines, 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
https://www.bioz.com/product/unaffected+control+pcs+201+010/CCD-1112Sk/pm29622803-126-7-9
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fibroblast lines - by Bioz Stars, 2026-09
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normal human dermal fibroblasts hdfn  (ATCC)
97
ATCC normal human dermal fibroblasts hdfn
Expression of wild-type (WT) and mutant transcripts in affected family members with the heterozygous c.618+836 T > G growth hormone receptor ( GHR ) 6Ω variant. The GHR 6Ω pseudoexon also diminishes GH-dependent STAT5B activation and accumulates extracellularly. A, Complementary DNA (cDNA) was prepared from dermal <t>fibroblasts</t> derived from a healthy control (HC) and patients 2 (P2) and P3 and both parents. Schematic showing the locations of the primers ( GHR cDNA exon 4F [forward] and GHR cDNA exon 8R [reverse] [blue arrows]) used to amplify the region encompassing WT GHR , the GHR 6Ω pseudoexon insertion. A “normal” 705–base pair (bp) polymerase chain reaction (PCR) product was seen in all samples. An additional larger (856-bp) PCR product was seen in P2, P3, and their mother, who were heterozygous for the c.618+836 T > G GHR 6Ω variant, indicating the additional 151-bp 6Ω pseudoexon insertion. B, Schematic showing the locations of the primers ( GHR cDNA pseudo F1 [forward] and GHR cDNA exon 8R [reverse] [blue arrows]). The forward primer at the junction of the 6Ω pseudoexon insertion means only sequences containing the GHR 6Ω pseudoexon insertion are amplified. The expected 387-bp PCR product is seen in patient 2, patient 3, and their mother, all of whom are heterozygous for the c.618+836 T > G GHR variant. C, Whole-cell lysates from untreated or GH-stimulated (20 minutes) HEK293 cells transfected with pcDNA3.1 empty vector, WT GHR or 6Ω GHR mutant constructs. Representative immunoblots of 3 experiments are shown. D, Immunoblot analysis of conditioned media with anti-GH binding protein (BP) antibody from HEK293 cells transfected with the 6Ω GHR mutant construct showing extracellular accumulation of the truncated mutant 6Ω GHR protein. B actin, β actin; K2M, kindred 2 mother; K2F kindred 2 father.
Normal Human Dermal Fibroblasts Hdfn, supplied by ATCC, 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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Image Search Results


Expression of wild-type (WT) and mutant transcripts in affected family members with the heterozygous c.618+836 T > G growth hormone receptor ( GHR ) 6Ω variant. The GHR 6Ω pseudoexon also diminishes GH-dependent STAT5B activation and accumulates extracellularly. A, Complementary DNA (cDNA) was prepared from dermal fibroblasts derived from a healthy control (HC) and patients 2 (P2) and P3 and both parents. Schematic showing the locations of the primers ( GHR cDNA exon 4F [forward] and GHR cDNA exon 8R [reverse] [blue arrows]) used to amplify the region encompassing WT GHR , the GHR 6Ω pseudoexon insertion. A “normal” 705–base pair (bp) polymerase chain reaction (PCR) product was seen in all samples. An additional larger (856-bp) PCR product was seen in P2, P3, and their mother, who were heterozygous for the c.618+836 T > G GHR 6Ω variant, indicating the additional 151-bp 6Ω pseudoexon insertion. B, Schematic showing the locations of the primers ( GHR cDNA pseudo F1 [forward] and GHR cDNA exon 8R [reverse] [blue arrows]). The forward primer at the junction of the 6Ω pseudoexon insertion means only sequences containing the GHR 6Ω pseudoexon insertion are amplified. The expected 387-bp PCR product is seen in patient 2, patient 3, and their mother, all of whom are heterozygous for the c.618+836 T > G GHR variant. C, Whole-cell lysates from untreated or GH-stimulated (20 minutes) HEK293 cells transfected with pcDNA3.1 empty vector, WT GHR or 6Ω GHR mutant constructs. Representative immunoblots of 3 experiments are shown. D, Immunoblot analysis of conditioned media with anti-GH binding protein (BP) antibody from HEK293 cells transfected with the 6Ω GHR mutant construct showing extracellular accumulation of the truncated mutant 6Ω GHR protein. B actin, β actin; K2M, kindred 2 mother; K2F kindred 2 father.

Journal: The Journal of Clinical Endocrinology and Metabolism

Article Title: Growth Hormone Receptor (GHR) 6Ω Pseudoexon Activation: A Novel Cause of Severe Growth Hormone Insensitivity

doi: 10.1210/clinem/dgab550

Figure Lengend Snippet: Expression of wild-type (WT) and mutant transcripts in affected family members with the heterozygous c.618+836 T > G growth hormone receptor ( GHR ) 6Ω variant. The GHR 6Ω pseudoexon also diminishes GH-dependent STAT5B activation and accumulates extracellularly. A, Complementary DNA (cDNA) was prepared from dermal fibroblasts derived from a healthy control (HC) and patients 2 (P2) and P3 and both parents. Schematic showing the locations of the primers ( GHR cDNA exon 4F [forward] and GHR cDNA exon 8R [reverse] [blue arrows]) used to amplify the region encompassing WT GHR , the GHR 6Ω pseudoexon insertion. A “normal” 705–base pair (bp) polymerase chain reaction (PCR) product was seen in all samples. An additional larger (856-bp) PCR product was seen in P2, P3, and their mother, who were heterozygous for the c.618+836 T > G GHR 6Ω variant, indicating the additional 151-bp 6Ω pseudoexon insertion. B, Schematic showing the locations of the primers ( GHR cDNA pseudo F1 [forward] and GHR cDNA exon 8R [reverse] [blue arrows]). The forward primer at the junction of the 6Ω pseudoexon insertion means only sequences containing the GHR 6Ω pseudoexon insertion are amplified. The expected 387-bp PCR product is seen in patient 2, patient 3, and their mother, all of whom are heterozygous for the c.618+836 T > G GHR variant. C, Whole-cell lysates from untreated or GH-stimulated (20 minutes) HEK293 cells transfected with pcDNA3.1 empty vector, WT GHR or 6Ω GHR mutant constructs. Representative immunoblots of 3 experiments are shown. D, Immunoblot analysis of conditioned media with anti-GH binding protein (BP) antibody from HEK293 cells transfected with the 6Ω GHR mutant construct showing extracellular accumulation of the truncated mutant 6Ω GHR protein. B actin, β actin; K2M, kindred 2 mother; K2F kindred 2 father.

Article Snippet: Primary dermal fibroblasts of normal human neonatal origin, (ATCC PCS201010) were used as controls.

Techniques: Expressing, Mutagenesis, Variant Assay, Activation Assay, Derivative Assay, Control, Polymerase Chain Reaction, Amplification, Transfection, Plasmid Preparation, Construct, Western Blot, Binding Assay