I think, uh, this mechanism is uh. Not universal for all the neuroblastoma cell line and patients. Uh, it can only be explained in a non-amplified cell lines and the, the corresponding patients.
I think, uh, this mechanism is uh. Not universal for all the neuroblastoma cell line and patients. Uh, it can only be explained in a non-amplified cell lines and the, the corresponding patients.
I think, uh, this mechanism is uh. Not universal for all the neuroblastoma cell line and patients. Uh, it can only be explained in a non-amplified cell lines and the, the corresponding patients.
I think, uh, this mechanism is uh. Not universal for all the neuroblastoma cell line and patients. Uh, it can only be explained in a non-amplified cell lines and the, the corresponding patients.
Dr. Yujie Ma - Best of the Best in Pediatric Surgery 2025
▶Ep 3 · 0:45
quoteNeuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympatho adrenal cells in neuro crest.↗
▶Ep 3 · 0:45
epidemiologicalNeuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympathoadrenal cells in neural crest.↗
▶Ep 3 · 0:45
quoteNeuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympatho adrenal cells in neuro crest.↗
▶Ep 3 · 0:45
epidemiologicalNeuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympathoadrenal cells in neural crest.↗
▶Ep 3 · 0:56
clinicalRetinoic acid is used to induce differentiation in treatment of high risk neuroblastoma.↗
▶Ep 3 · 0:56
clinicalRetinoic acid is used to induce differentiation in treatment of high risk neuroblastoma.↗
▶Ep 3 · 1:03
clinicalRetinoic acid efficacy varies in patients due to the highly heterogeneous nature of neuroblastoma.↗
▶Ep 3 · 1:03
clinicalRetinoic acid efficacy varies in patients due to the highly heterogeneous nature of neuroblastoma.↗
▶Ep 3 · 1:19
clinicalPCP4 was identified as one of the differentiation markers of neuroblastoma tumor cells in a previous Cancer Cell publication.↗
▶Ep 3 · 1:19
clinicalPCP4 was identified as one of the differentiation markers of neuroblastoma tumor cells in a previous Cancer Cell publication.↗
▶Ep 3 · 1:38
clinicalPCP4 modulates the rate of calcium binding to calmodulin, which is a critical step in activating calmodulin dependent kinase.↗
▶Ep 3 · 1:38
quotePCP4 modulates the rate of calcium binding to camodulin, which is a critical step in activating camodulin dependent kinase.↗
▶Ep 3 · 1:38
clinicalPCP4 modulates the rate of calcium binding to calmodulin, which is a critical step in activating calmodulin dependent kinase.↗
▶Ep 3 · 1:38
quotePCP4 modulates the rate of calcium binding to camodulin, which is a critical step in activating camodulin dependent kinase.↗
▶Ep 3 · 1:49
clinicalThe binding of PCP4 with calmodulin was verified in neuroblastoma by co-immunoprecipitation.↗
▶Ep 3 · 1:49
clinicalCAMK2G was identified as a target kinase of calmodulin using mass spectrometry.↗
▶Ep 3 · 1:49
clinicalThe binding of PCP4 with calmodulin was verified in neuroblastoma by co-immunoprecipitation.↗
▶Ep 3 · 1:49
clinicalCAMK2G was identified as a target kinase of calmodulin using mass spectrometry.↗
▶Ep 3 · 2:06
clinicalCAMK2G is a member of the serine/threonine protein kinase family.↗
▶Ep 3 · 2:06
clinicalCAMK2G is a member of the serine/threonine protein kinase family.↗
▶Ep 3 · 2:10
clinicalCAMK2G plays an important role in neuronal development and synaptic plasticity.↗
▶Ep 3 · 2:10
clinicalCAMK2G plays an important role in neuronal development and synaptic plasticity.↗
▶Ep 3 · 2:24
clinicalWhen CAMK2G is activated by calmodulin, it gets autophosphorylated at the site of threonine 287.↗
▶Ep 3 · 2:24
clinicalWhen CAMK2G is activated by calmodulin, it gets autophosphorylated at the site of threonine 287.↗
▶Ep 3 · 2:33
clinicalPCP4 overexpression upregulated the threonine 287 phosphorylation of CAMK2G in neuroblastoma cells.↗
▶Ep 3 · 2:33
clinicalPCP4 overexpression upregulated the threonine 287 phosphorylation of CAMK2G in neuroblastoma cells.↗
▶Ep 3 · 3:02
clinicalLow CAMK2G mRNA expression was associated with worse overall and event-free survival in neuroblastoma patients.↗
▶Ep 3 · 3:02
clinicalLow CAMK2G expression was associated with advanced INSS stages and unfavorable histology in neuroblastoma.↗
▶Ep 3 · 3:02
clinicalLow CAMK2G expression was associated with advanced INSS stages and unfavorable histology in neuroblastoma.↗
▶Ep 3 · 3:02
clinicalLow CAMK2G mRNA expression was associated with worse overall and event-free survival in neuroblastoma patients.↗
▶Ep 3 · 3:14
clinicalLow CAMK2G expression was associated with MYCN amplified status, high risk, and tumor progression in neuroblastoma.↗
▶Ep 3 · 3:14
clinicalLow CAMK2G expression was associated with MYCN amplified status, high risk, and tumor progression in neuroblastoma.↗
▶Ep 3 · 3:30
clinicalCAMK2G knockdown in SKNSH cells resulted in inhibited neurite outgrowth even under retinoic acid induction.↗
▶Ep 3 · 3:30
clinicalCAMK2G knockdown in SKNSH cells resulted in inhibited neurite outgrowth even under retinoic acid induction.↗
▶Ep 3 · 3:44
clinicalExpression of neuronal differentiation markers were downregulated following CAMK2G knockdown.↗
▶Ep 3 · 3:44
clinicalExpression of neuronal differentiation markers were downregulated following CAMK2G knockdown.↗
▶Ep 3 · 3:58
clinicalGene enrichment analysis of downregulated genes following CAMK2G knockdown showed enriched terms related to neuronal differentiation including synaptic signaling, plasma membrane, and ion channel activity.↗
▶Ep 3 · 3:58
clinicalGene enrichment analysis of downregulated genes following CAMK2G knockdown showed enriched terms related to neuronal differentiation including synaptic signaling, plasma membrane, and ion channel activity.↗
▶Ep 3 · 4:13
clinicalCAMK2G knockdown promoted migration and invasion of neuroblastoma cells as shown by transwell assays.↗
▶Ep 3 · 4:13
clinicalCAMK2G knockdown promoted migration and invasion of neuroblastoma cells as shown by transwell assays.↗
▶Ep 3 · 4:21
clinicalKEGG analysis of upregulated genes following CAMK2G knockdown identified enriched pathways associated with tumor migration and invasion, including extracellular matrix receptor interaction, focal adhesion, and regulation of actin cytoskeleton.↗
▶Ep 3 · 4:21
clinicalKEGG analysis of upregulated genes following CAMK2G knockdown identified enriched pathways associated with tumor migration and invasion, including extracellular matrix receptor interaction, focal adhesion, and regulation of actin cytoskeleton.↗
▶Ep 3 · 6:20
clinicalCAMK2G is expressed at low levels in SKNSH neuroblastoma cell line.↗
▶Ep 3 · 6:20
clinicalCAMK2G is expressed at low levels in SKNSH neuroblastoma cell line.↗
▶Ep 3 · 6:33
clinicalCAMK2G is highly expressed in BE2 and SKNS neuroblastoma cell lines, which are MYCN amplified cell lines.↗
▶Ep 3 · 6:33
clinicalCAMK2G function is not strong enough to overcome the oncogenic function of MYCN in MYCN-amplified neuroblastoma cell lines.↗
▶Ep 3 · 6:33
clinicalCAMK2G function is not strong enough to overcome the oncogenic function of MYCN in MYCN-amplified neuroblastoma cell lines.↗
▶Ep 3 · 6:33
clinicalCAMK2G is highly expressed in BE2 and SKNS neuroblastoma cell lines, which are MYCN amplified cell lines.↗
▶Ep 3 · 7:11
clinicalCAMK2G did not regulate neuronal differentiation in MYCN-amplified neuroblastoma cell lines.↗
▶Ep 3 · 7:11
clinicalCAMK2G did not regulate neuronal differentiation in MYCN-amplified neuroblastoma cell lines.↗
▶Ep 3 · 7:33
quoteI think, uh, this mechanism is uh. Not universal for all the neuroblastoma cell line and patients. Uh, it can only be explained in a non-amplified cell lines and the, the corresponding patients.↗
▶Ep 3 · 7:33
quoteI think, uh, this mechanism is uh. Not universal for all the neuroblastoma cell line and patients. Uh, it can only be explained in a non-amplified cell lines and the, the corresponding patients.↗
▶Ep 3 · 7:33
opinionThe CAMK2G differentiation mechanism is not universal for all neuroblastoma cell lines and patients, and can only be explained in MYCN non-amplified cell lines and corresponding patients.↗
▶Ep 3 · 7:33
opinionThe CAMK2G differentiation mechanism is not universal for all neuroblastoma cell lines and patients, and can only be explained in MYCN non-amplified cell lines and corresponding patients.↗
Dr. Yujie Ma - Best of the Best in Pediatric Surgery 2025
▶Ep 18 · 0:45
quoteNeuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympatho adrenal cells in neuro crest.↗
▶Ep 18 · 0:45
quoteNeuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympatho adrenal cells in neuro crest.↗
▶Ep 18 · 0:45
epidemiologicalNeuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympathoadrenal cells in neural crest.↗
▶Ep 18 · 0:45
epidemiologicalNeuroblastoma is the most common extracranial solid tumor of childhood arising from aberrant differentiation of sympathoadrenal cells in neural crest.↗
▶Ep 18 · 0:56
clinicalRetinoic acid is used to induce differentiation in treatment of high risk neuroblastoma.↗
▶Ep 18 · 0:56
clinicalRetinoic acid is used to induce differentiation in treatment of high risk neuroblastoma.↗
▶Ep 18 · 1:03
clinicalRetinoic acid efficacy varies in patients due to the highly heterogeneous nature of neuroblastoma.↗
▶Ep 18 · 1:03
clinicalRetinoic acid efficacy varies in patients due to the highly heterogeneous nature of neuroblastoma.↗
▶Ep 18 · 1:19
clinicalPCP4 was identified as one of the differentiation markers of neuroblastoma tumor cells in a previous Cancer Cell publication.↗
▶Ep 18 · 1:19
clinicalPCP4 was identified as one of the differentiation markers of neuroblastoma tumor cells in a previous Cancer Cell publication.↗
▶Ep 18 · 1:38
quotePCP4 modulates the rate of calcium binding to camodulin, which is a critical step in activating camodulin dependent kinase.↗
▶Ep 18 · 1:38
quotePCP4 modulates the rate of calcium binding to camodulin, which is a critical step in activating camodulin dependent kinase.↗
▶Ep 18 · 1:38
clinicalPCP4 modulates the rate of calcium binding to calmodulin, which is a critical step in activating calmodulin dependent kinase.↗
▶Ep 18 · 1:38
clinicalPCP4 modulates the rate of calcium binding to calmodulin, which is a critical step in activating calmodulin dependent kinase.↗
▶Ep 18 · 1:49
clinicalThe binding of PCP4 with calmodulin was verified in neuroblastoma by co-immunoprecipitation.↗
▶Ep 18 · 1:49
clinicalCAMK2G was identified as a target kinase of calmodulin using mass spectrometry.↗
▶Ep 18 · 1:49
clinicalCAMK2G was identified as a target kinase of calmodulin using mass spectrometry.↗
▶Ep 18 · 1:49
clinicalThe binding of PCP4 with calmodulin was verified in neuroblastoma by co-immunoprecipitation.↗
▶Ep 18 · 2:06
clinicalCAMK2G is a member of the serine/threonine protein kinase family.↗
▶Ep 18 · 2:06
clinicalCAMK2G is a member of the serine/threonine protein kinase family.↗
▶Ep 18 · 2:10
clinicalCAMK2G plays an important role in neuronal development and synaptic plasticity.↗
▶Ep 18 · 2:10
clinicalCAMK2G plays an important role in neuronal development and synaptic plasticity.↗
▶Ep 18 · 2:24
clinicalWhen CAMK2G is activated by calmodulin, it gets autophosphorylated at the site of threonine 287.↗
▶Ep 18 · 2:24
clinicalWhen CAMK2G is activated by calmodulin, it gets autophosphorylated at the site of threonine 287.↗
▶Ep 18 · 2:33
clinicalPCP4 overexpression upregulated the threonine 287 phosphorylation of CAMK2G in neuroblastoma cells.↗
▶Ep 18 · 2:33
clinicalPCP4 overexpression upregulated the threonine 287 phosphorylation of CAMK2G in neuroblastoma cells.↗
▶Ep 18 · 3:02
clinicalLow CAMK2G mRNA expression was associated with worse overall and event-free survival in neuroblastoma patients.↗
▶Ep 18 · 3:02
clinicalLow CAMK2G expression was associated with advanced INSS stages and unfavorable histology in neuroblastoma.↗
▶Ep 18 · 3:02
clinicalLow CAMK2G expression was associated with advanced INSS stages and unfavorable histology in neuroblastoma.↗
▶Ep 18 · 3:02
clinicalLow CAMK2G mRNA expression was associated with worse overall and event-free survival in neuroblastoma patients.↗
▶Ep 18 · 3:14
clinicalLow CAMK2G expression was associated with MYCN amplified status, high risk, and tumor progression in neuroblastoma.↗
▶Ep 18 · 3:14
clinicalLow CAMK2G expression was associated with MYCN amplified status, high risk, and tumor progression in neuroblastoma.↗
▶Ep 18 · 3:30
clinicalCAMK2G knockdown in SKNSH cells resulted in inhibited neurite outgrowth even under retinoic acid induction.↗
▶Ep 18 · 3:30
clinicalCAMK2G knockdown in SKNSH cells resulted in inhibited neurite outgrowth even under retinoic acid induction.↗
▶Ep 18 · 3:44
clinicalExpression of neuronal differentiation markers were downregulated following CAMK2G knockdown.↗
▶Ep 18 · 3:44
clinicalExpression of neuronal differentiation markers were downregulated following CAMK2G knockdown.↗
▶Ep 18 · 3:58
clinicalGene enrichment analysis of downregulated genes following CAMK2G knockdown showed enriched terms related to neuronal differentiation including synaptic signaling, plasma membrane, and ion channel activity.↗
▶Ep 18 · 3:58
clinicalGene enrichment analysis of downregulated genes following CAMK2G knockdown showed enriched terms related to neuronal differentiation including synaptic signaling, plasma membrane, and ion channel activity.↗
▶Ep 18 · 4:13
clinicalCAMK2G knockdown promoted migration and invasion of neuroblastoma cells as shown by transwell assays.↗
▶Ep 18 · 4:13
clinicalCAMK2G knockdown promoted migration and invasion of neuroblastoma cells as shown by transwell assays.↗
▶Ep 18 · 4:21
clinicalKEGG analysis of upregulated genes following CAMK2G knockdown identified enriched pathways associated with tumor migration and invasion, including extracellular matrix receptor interaction, focal adhesion, and regulation of actin cytoskeleton.↗
▶Ep 18 · 4:21
clinicalKEGG analysis of upregulated genes following CAMK2G knockdown identified enriched pathways associated with tumor migration and invasion, including extracellular matrix receptor interaction, focal adhesion, and regulation of actin cytoskeleton.↗
▶Ep 18 · 6:20
clinicalCAMK2G is expressed at low levels in SKNSH neuroblastoma cell line.↗
▶Ep 18 · 6:20
clinicalCAMK2G is expressed at low levels in SKNSH neuroblastoma cell line.↗
▶Ep 18 · 6:33
clinicalCAMK2G is highly expressed in BE2 and SKNS neuroblastoma cell lines, which are MYCN amplified cell lines.↗
▶Ep 18 · 6:33
clinicalCAMK2G function is not strong enough to overcome the oncogenic function of MYCN in MYCN-amplified neuroblastoma cell lines.↗
▶Ep 18 · 6:33
clinicalCAMK2G is highly expressed in BE2 and SKNS neuroblastoma cell lines, which are MYCN amplified cell lines.↗
▶Ep 18 · 6:33
clinicalCAMK2G function is not strong enough to overcome the oncogenic function of MYCN in MYCN-amplified neuroblastoma cell lines.↗
▶Ep 18 · 7:11
clinicalCAMK2G did not regulate neuronal differentiation in MYCN-amplified neuroblastoma cell lines.↗
▶Ep 18 · 7:11
clinicalCAMK2G did not regulate neuronal differentiation in MYCN-amplified neuroblastoma cell lines.↗
▶Ep 18 · 7:33
opinionThe CAMK2G differentiation mechanism is not universal for all neuroblastoma cell lines and patients, and can only be explained in MYCN non-amplified cell lines and corresponding patients.↗
▶Ep 18 · 7:33
quoteI think, uh, this mechanism is uh. Not universal for all the neuroblastoma cell line and patients. Uh, it can only be explained in a non-amplified cell lines and the, the corresponding patients.↗
▶Ep 18 · 7:33
opinionThe CAMK2G differentiation mechanism is not universal for all neuroblastoma cell lines and patients, and can only be explained in MYCN non-amplified cell lines and corresponding patients.↗
▶Ep 18 · 7:33
quoteI think, uh, this mechanism is uh. Not universal for all the neuroblastoma cell line and patients. Uh, it can only be explained in a non-amplified cell lines and the, the corresponding patients.↗
