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Biotechnology Information microarray gene expression datasets
Microarray Gene Expression Datasets, supplied by Biotechnology Information, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Microarray:

Article Title: Possible involvement of tubular interleukin-34 in macrophage recruitment during colistin-induced nephrotoxicity in rats.
Article Snippet: .. Complete microarray data have been submitted and are readily retrievable from the public database National Center for Biotechnology Information Vol. ..

Article Title: Genetic underpinnings of type-2 diabetes (T2D) with colorectal cancer (CRC): In-silico discovery of common molecular signatures, pathogenetic processes and therapeutic candidates
Article Snippet: .. Two microarray gene expression datasets for each of T2D and CRC were downloaded from the Gene Expression Omnibus (GEO) repository of the National Center for Biotechnology Information (NCBI). ..

Article Title: Genetic underpinnings of type-2 diabetes (T2D) with colorectal cancer (CRC): In-silico discovery of common molecular signatures, pathogenetic processes and therapeutic candidates.
Article Snippet: .. Two microarray gene expression datasets for each of T2D and CRC were downloaded from the Gene Expression Omnibus (GEO) repository of the National Center for Biotechnology Information (NCBI). ..

Article Title: AI guided discovery of a murine model of asymptomatic Alzheimer’s disease
Article Snippet: .. Publicly available microarray and RNA-sequencing datasets were obtained from the National Center for Biotechnology Information (NCBI) Gene Expression Omnibus (GEO) repository [ – ]. .. For Affymetrix microarray platforms, raw intensity files were normalized using Robust Multichip Average (RMA) [ ].

Article Title: cIAP1 inhibitor of apoptosis is a tumor suppressor in Ewing sarcoma.
Article Snippet: Ewing sarcoma (EwS) is a highly aggressive pediatric malignancy driven by EWSR1::ETS fusion oncoproteins –primarily EWSR1::FLI1– which deregulate genes essential for differentiation, proliferation, and cell survival.. To uncover key downstream targets of this fusion involved in cell differentiation, we combined transcriptomic profiling of EwS cell lines following EWSR1::ETS inhibition with gene ontology analysis, a clinically annotated gene expression dataset derived from EwS patient material and network analyses.. This integrative approach identified inhibitor of apoptosis protein 1 (cIAP1, alias BIRC2) as an EWSR1::FLI1-suppressed gene.

Article Title: Zfand5 terminates TLR3/4 signaling and necroptosis by targeting TRIF to the proteasome for degradation.
Article Snippet: .. Given that PRR-driven innate immune response must be tightly regulated to ensure proper initiation and resolution of inflammation (42), we investigated how macrophages respond to the TLR4 agonist lipopolysaccharide (LPS) by analyzing publicly available microarray data from the National Center for Biotechnology Information (NCBI). ..

Article Title: Small proline-rich protein 1A is a novel target of peroxisome proliferator-activated receptor gamma in steatotic liver disease.
Article Snippet: Peroxisome proliferator-activated receptor gamma (PPARγ) is a central regulator of lipid homeostasis; however, the specific downstream effectors mediating hepatic steatosis remain incompletely defined.. In this study, we investigated the molecular basis, by which PPARγ regulates the expression of small proline-rich protein 1 A (SPRR1A) during the development of fatty liver.. We initially performed a bioinformatic re-analysis of publicly available microarray datasets to characterize the gene expression profiles associated with hepatic steatosis in leptin-deficient type 2 diabetic (ob/ob) mice and patients with metabolic dysfunction–associated steatotic liver disease (MASLD).

Article Title: Identification of susceptibility modules and genes through WGCNA and ceRNA network analysis in neuropathic pain-induced anxiodepression.
Article Snippet: .. The microarray data under access number GSE92718 were downloaded from the National Center of Biotechnology Information (NCBI) Gene Expression Omnibus (GEO; www.ncbi.nlm.nih.gov/). ..

Gene Expression:

Article Title: Genetic underpinnings of type-2 diabetes (T2D) with colorectal cancer (CRC): In-silico discovery of common molecular signatures, pathogenetic processes and therapeutic candidates
Article Snippet: .. Two microarray gene expression datasets for each of T2D and CRC were downloaded from the Gene Expression Omnibus (GEO) repository of the National Center for Biotechnology Information (NCBI). ..

Article Title: Genetic underpinnings of type-2 diabetes (T2D) with colorectal cancer (CRC): In-silico discovery of common molecular signatures, pathogenetic processes and therapeutic candidates.
Article Snippet: .. Two microarray gene expression datasets for each of T2D and CRC were downloaded from the Gene Expression Omnibus (GEO) repository of the National Center for Biotechnology Information (NCBI). ..

Article Title: AI guided discovery of a murine model of asymptomatic Alzheimer’s disease
Article Snippet: .. Publicly available microarray and RNA-sequencing datasets were obtained from the National Center for Biotechnology Information (NCBI) Gene Expression Omnibus (GEO) repository [ – ]. .. For Affymetrix microarray platforms, raw intensity files were normalized using Robust Multichip Average (RMA) [ ].

Article Title: Identification of susceptibility modules and genes through WGCNA and ceRNA network analysis in neuropathic pain-induced anxiodepression.
Article Snippet: .. The microarray data under access number GSE92718 were downloaded from the National Center of Biotechnology Information (NCBI) Gene Expression Omnibus (GEO; www.ncbi.nlm.nih.gov/). ..

RNA sequencing:

Article Title: AI guided discovery of a murine model of asymptomatic Alzheimer’s disease
Article Snippet: .. Publicly available microarray and RNA-sequencing datasets were obtained from the National Center for Biotechnology Information (NCBI) Gene Expression Omnibus (GEO) repository [ – ]. .. For Affymetrix microarray platforms, raw intensity files were normalized using Robust Multichip Average (RMA) [ ].



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PER2 integrates <t>circadian</t> and transcriptional signals at the mouse Esr1 promoter. ( A ) Time-course <t>expression</t> profiles of Esr1 and Per2 mRNA showing circadian oscillations in multiple mouse tissues. Wild-type mice were entrained to 12-h light:12-h dark cycles for one week, then released into constant darkness. Tissues (white adipose tissue, liver, and kidney) were collected at 2 h intervals for 48 h mRNA expression levels (normalized counts) are plotted against circadian time (CT). Fitted cosine curves (blue for Esr1 , red for Per2 ) show that both <t>genes</t> oscillate with similar periodicity across tissues, with tissue-specific phase relationships. ( B ) Quantitative circadian parameters (period, phase, amplitude, and baseline expression) determined by meta2d analysis of data shown in panel A. Upper table. Circadian periods for Esr1 and Per2 in each tissue show remarkable similarity (white adipose: ∼24.2 h for both; liver: ∼23.8 h Esr1 , ∼23.5 h Per2 ; kidney: ∼24.1 h for both). Lower table. Phase analysis reveals tissue-specific phase relationships: Esr1 leads Per2 by 2–4 h in white adipose tissue and kidney, while lagging by ∼1–2 h in liver. P-values (p < 0.01) confirm statistically significant rhythmicity for both genes in all tissues. ( C ) Per2 and Esr1 circadian rhythms are abolished in Per1 −/− / Per2 −/− double knockout mice. Liver expression data from wild-type and Per1/2 dKO mice ( GSE171975 ) show that in wild-type liver, both Per2 and Esr1 exhibit robust circadian oscillations (period ∼23 h, p < 0.01). In contrast, both genes completely lose rhythmicity in Per1/2 dKO liver tissue, with expression remaining flat across all time points. Importantly, basal transcript levels are maintained despite loss of oscillation, demonstrating that Esr1 transcription per se does not require functional PER proteins, but rather that circadian modulation of expression requires clock function. ( D ) Pou2f1 and Brca1 transcripts show no circadian rhythmicity at the mRNA level. Upper panel: Pou2f1 expression remains relatively constant across the circadian cycle in both wild-type and Per1/2 dKO liver, with no statistically significant oscillations. Lower panel: Brca1 expression similarly lacks circadian rhythmicity in both genotypes. These non-rhythmic expression patterns contrast sharply with the robust oscillations observed for Per2 and Esr1 , suggesting that constitutively expressed POU2F1(OCT-1) and BRCA1 serve as stable scaffolding factors that cooperate with rhythmically expressed PER2 to impose circadian control on Esr1 transcription. ( E ) Meta2d analysis results for Brca1 and Pou2f1 showing circadian parameters and statistical assessment. p-values confirm the absence of significant circadian rhythmicity (p > 0.01) for both genes in both wild-type and Per1/2 dKO animals. ( F ) Direct temporal comparison of Per2 and Esr1 oscillations in wild-type and Per1/2 dKO liver. Per2 (red) and Esr1 (blue) expression from GSE171975 are plotted together to visualize their temporal relationship.
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PER2 integrates <t>circadian</t> and transcriptional signals at the mouse Esr1 promoter. ( A ) Time-course <t>expression</t> profiles of Esr1 and Per2 mRNA showing circadian oscillations in multiple mouse tissues. Wild-type mice were entrained to 12-h light:12-h dark cycles for one week, then released into constant darkness. Tissues (white adipose tissue, liver, and kidney) were collected at 2 h intervals for 48 h mRNA expression levels (normalized counts) are plotted against circadian time (CT). Fitted cosine curves (blue for Esr1 , red for Per2 ) show that both <t>genes</t> oscillate with similar periodicity across tissues, with tissue-specific phase relationships. ( B ) Quantitative circadian parameters (period, phase, amplitude, and baseline expression) determined by meta2d analysis of data shown in panel A. Upper table. Circadian periods for Esr1 and Per2 in each tissue show remarkable similarity (white adipose: ∼24.2 h for both; liver: ∼23.8 h Esr1 , ∼23.5 h Per2 ; kidney: ∼24.1 h for both). Lower table. Phase analysis reveals tissue-specific phase relationships: Esr1 leads Per2 by 2–4 h in white adipose tissue and kidney, while lagging by ∼1–2 h in liver. P-values (p < 0.01) confirm statistically significant rhythmicity for both genes in all tissues. ( C ) Per2 and Esr1 circadian rhythms are abolished in Per1 −/− / Per2 −/− double knockout mice. Liver expression data from wild-type and Per1/2 dKO mice ( GSE171975 ) show that in wild-type liver, both Per2 and Esr1 exhibit robust circadian oscillations (period ∼23 h, p < 0.01). In contrast, both genes completely lose rhythmicity in Per1/2 dKO liver tissue, with expression remaining flat across all time points. Importantly, basal transcript levels are maintained despite loss of oscillation, demonstrating that Esr1 transcription per se does not require functional PER proteins, but rather that circadian modulation of expression requires clock function. ( D ) Pou2f1 and Brca1 transcripts show no circadian rhythmicity at the mRNA level. Upper panel: Pou2f1 expression remains relatively constant across the circadian cycle in both wild-type and Per1/2 dKO liver, with no statistically significant oscillations. Lower panel: Brca1 expression similarly lacks circadian rhythmicity in both genotypes. These non-rhythmic expression patterns contrast sharply with the robust oscillations observed for Per2 and Esr1 , suggesting that constitutively expressed POU2F1(OCT-1) and BRCA1 serve as stable scaffolding factors that cooperate with rhythmically expressed PER2 to impose circadian control on Esr1 transcription. ( E ) Meta2d analysis results for Brca1 and Pou2f1 showing circadian parameters and statistical assessment. p-values confirm the absence of significant circadian rhythmicity (p > 0.01) for both genes in both wild-type and Per1/2 dKO animals. ( F ) Direct temporal comparison of Per2 and Esr1 oscillations in wild-type and Per1/2 dKO liver. Per2 (red) and Esr1 (blue) expression from GSE171975 are plotted together to visualize their temporal relationship.
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PER2 integrates <t>circadian</t> and transcriptional signals at the mouse Esr1 promoter. ( A ) Time-course <t>expression</t> profiles of Esr1 and Per2 mRNA showing circadian oscillations in multiple mouse tissues. Wild-type mice were entrained to 12-h light:12-h dark cycles for one week, then released into constant darkness. Tissues (white adipose tissue, liver, and kidney) were collected at 2 h intervals for 48 h mRNA expression levels (normalized counts) are plotted against circadian time (CT). Fitted cosine curves (blue for Esr1 , red for Per2 ) show that both <t>genes</t> oscillate with similar periodicity across tissues, with tissue-specific phase relationships. ( B ) Quantitative circadian parameters (period, phase, amplitude, and baseline expression) determined by meta2d analysis of data shown in panel A. Upper table. Circadian periods for Esr1 and Per2 in each tissue show remarkable similarity (white adipose: ∼24.2 h for both; liver: ∼23.8 h Esr1 , ∼23.5 h Per2 ; kidney: ∼24.1 h for both). Lower table. Phase analysis reveals tissue-specific phase relationships: Esr1 leads Per2 by 2–4 h in white adipose tissue and kidney, while lagging by ∼1–2 h in liver. P-values (p < 0.01) confirm statistically significant rhythmicity for both genes in all tissues. ( C ) Per2 and Esr1 circadian rhythms are abolished in Per1 −/− / Per2 −/− double knockout mice. Liver expression data from wild-type and Per1/2 dKO mice ( GSE171975 ) show that in wild-type liver, both Per2 and Esr1 exhibit robust circadian oscillations (period ∼23 h, p < 0.01). In contrast, both genes completely lose rhythmicity in Per1/2 dKO liver tissue, with expression remaining flat across all time points. Importantly, basal transcript levels are maintained despite loss of oscillation, demonstrating that Esr1 transcription per se does not require functional PER proteins, but rather that circadian modulation of expression requires clock function. ( D ) Pou2f1 and Brca1 transcripts show no circadian rhythmicity at the mRNA level. Upper panel: Pou2f1 expression remains relatively constant across the circadian cycle in both wild-type and Per1/2 dKO liver, with no statistically significant oscillations. Lower panel: Brca1 expression similarly lacks circadian rhythmicity in both genotypes. These non-rhythmic expression patterns contrast sharply with the robust oscillations observed for Per2 and Esr1 , suggesting that constitutively expressed POU2F1(OCT-1) and BRCA1 serve as stable scaffolding factors that cooperate with rhythmically expressed PER2 to impose circadian control on Esr1 transcription. ( E ) Meta2d analysis results for Brca1 and Pou2f1 showing circadian parameters and statistical assessment. p-values confirm the absence of significant circadian rhythmicity (p > 0.01) for both genes in both wild-type and Per1/2 dKO animals. ( F ) Direct temporal comparison of Per2 and Esr1 oscillations in wild-type and Per1/2 dKO liver. Per2 (red) and Esr1 (blue) expression from GSE171975 are plotted together to visualize their temporal relationship.
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PER2 integrates <t>circadian</t> and transcriptional signals at the mouse Esr1 promoter. ( A ) Time-course <t>expression</t> profiles of Esr1 and Per2 mRNA showing circadian oscillations in multiple mouse tissues. Wild-type mice were entrained to 12-h light:12-h dark cycles for one week, then released into constant darkness. Tissues (white adipose tissue, liver, and kidney) were collected at 2 h intervals for 48 h mRNA expression levels (normalized counts) are plotted against circadian time (CT). Fitted cosine curves (blue for Esr1 , red for Per2 ) show that both <t>genes</t> oscillate with similar periodicity across tissues, with tissue-specific phase relationships. ( B ) Quantitative circadian parameters (period, phase, amplitude, and baseline expression) determined by meta2d analysis of data shown in panel A. Upper table. Circadian periods for Esr1 and Per2 in each tissue show remarkable similarity (white adipose: ∼24.2 h for both; liver: ∼23.8 h Esr1 , ∼23.5 h Per2 ; kidney: ∼24.1 h for both). Lower table. Phase analysis reveals tissue-specific phase relationships: Esr1 leads Per2 by 2–4 h in white adipose tissue and kidney, while lagging by ∼1–2 h in liver. P-values (p < 0.01) confirm statistically significant rhythmicity for both genes in all tissues. ( C ) Per2 and Esr1 circadian rhythms are abolished in Per1 −/− / Per2 −/− double knockout mice. Liver expression data from wild-type and Per1/2 dKO mice ( GSE171975 ) show that in wild-type liver, both Per2 and Esr1 exhibit robust circadian oscillations (period ∼23 h, p < 0.01). In contrast, both genes completely lose rhythmicity in Per1/2 dKO liver tissue, with expression remaining flat across all time points. Importantly, basal transcript levels are maintained despite loss of oscillation, demonstrating that Esr1 transcription per se does not require functional PER proteins, but rather that circadian modulation of expression requires clock function. ( D ) Pou2f1 and Brca1 transcripts show no circadian rhythmicity at the mRNA level. Upper panel: Pou2f1 expression remains relatively constant across the circadian cycle in both wild-type and Per1/2 dKO liver, with no statistically significant oscillations. Lower panel: Brca1 expression similarly lacks circadian rhythmicity in both genotypes. These non-rhythmic expression patterns contrast sharply with the robust oscillations observed for Per2 and Esr1 , suggesting that constitutively expressed POU2F1(OCT-1) and BRCA1 serve as stable scaffolding factors that cooperate with rhythmically expressed PER2 to impose circadian control on Esr1 transcription. ( E ) Meta2d analysis results for Brca1 and Pou2f1 showing circadian parameters and statistical assessment. p-values confirm the absence of significant circadian rhythmicity (p > 0.01) for both genes in both wild-type and Per1/2 dKO animals. ( F ) Direct temporal comparison of Per2 and Esr1 oscillations in wild-type and Per1/2 dKO liver. Per2 (red) and Esr1 (blue) expression from GSE171975 are plotted together to visualize their temporal relationship.
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PER2 integrates <t>circadian</t> and transcriptional signals at the mouse Esr1 promoter. ( A ) Time-course <t>expression</t> profiles of Esr1 and Per2 mRNA showing circadian oscillations in multiple mouse tissues. Wild-type mice were entrained to 12-h light:12-h dark cycles for one week, then released into constant darkness. Tissues (white adipose tissue, liver, and kidney) were collected at 2 h intervals for 48 h mRNA expression levels (normalized counts) are plotted against circadian time (CT). Fitted cosine curves (blue for Esr1 , red for Per2 ) show that both <t>genes</t> oscillate with similar periodicity across tissues, with tissue-specific phase relationships. ( B ) Quantitative circadian parameters (period, phase, amplitude, and baseline expression) determined by meta2d analysis of data shown in panel A. Upper table. Circadian periods for Esr1 and Per2 in each tissue show remarkable similarity (white adipose: ∼24.2 h for both; liver: ∼23.8 h Esr1 , ∼23.5 h Per2 ; kidney: ∼24.1 h for both). Lower table. Phase analysis reveals tissue-specific phase relationships: Esr1 leads Per2 by 2–4 h in white adipose tissue and kidney, while lagging by ∼1–2 h in liver. P-values (p < 0.01) confirm statistically significant rhythmicity for both genes in all tissues. ( C ) Per2 and Esr1 circadian rhythms are abolished in Per1 −/− / Per2 −/− double knockout mice. Liver expression data from wild-type and Per1/2 dKO mice ( GSE171975 ) show that in wild-type liver, both Per2 and Esr1 exhibit robust circadian oscillations (period ∼23 h, p < 0.01). In contrast, both genes completely lose rhythmicity in Per1/2 dKO liver tissue, with expression remaining flat across all time points. Importantly, basal transcript levels are maintained despite loss of oscillation, demonstrating that Esr1 transcription per se does not require functional PER proteins, but rather that circadian modulation of expression requires clock function. ( D ) Pou2f1 and Brca1 transcripts show no circadian rhythmicity at the mRNA level. Upper panel: Pou2f1 expression remains relatively constant across the circadian cycle in both wild-type and Per1/2 dKO liver, with no statistically significant oscillations. Lower panel: Brca1 expression similarly lacks circadian rhythmicity in both genotypes. These non-rhythmic expression patterns contrast sharply with the robust oscillations observed for Per2 and Esr1 , suggesting that constitutively expressed POU2F1(OCT-1) and BRCA1 serve as stable scaffolding factors that cooperate with rhythmically expressed PER2 to impose circadian control on Esr1 transcription. ( E ) Meta2d analysis results for Brca1 and Pou2f1 showing circadian parameters and statistical assessment. p-values confirm the absence of significant circadian rhythmicity (p > 0.01) for both genes in both wild-type and Per1/2 dKO animals. ( F ) Direct temporal comparison of Per2 and Esr1 oscillations in wild-type and Per1/2 dKO liver. Per2 (red) and Esr1 (blue) expression from GSE171975 are plotted together to visualize their temporal relationship.
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Biotechnology Information gene expression datasets
PER2 integrates <t>circadian</t> and transcriptional signals at the mouse Esr1 promoter. ( A ) Time-course <t>expression</t> profiles of Esr1 and Per2 mRNA showing circadian oscillations in multiple mouse tissues. Wild-type mice were entrained to 12-h light:12-h dark cycles for one week, then released into constant darkness. Tissues (white adipose tissue, liver, and kidney) were collected at 2 h intervals for 48 h mRNA expression levels (normalized counts) are plotted against circadian time (CT). Fitted cosine curves (blue for Esr1 , red for Per2 ) show that both <t>genes</t> oscillate with similar periodicity across tissues, with tissue-specific phase relationships. ( B ) Quantitative circadian parameters (period, phase, amplitude, and baseline expression) determined by meta2d analysis of data shown in panel A. Upper table. Circadian periods for Esr1 and Per2 in each tissue show remarkable similarity (white adipose: ∼24.2 h for both; liver: ∼23.8 h Esr1 , ∼23.5 h Per2 ; kidney: ∼24.1 h for both). Lower table. Phase analysis reveals tissue-specific phase relationships: Esr1 leads Per2 by 2–4 h in white adipose tissue and kidney, while lagging by ∼1–2 h in liver. P-values (p < 0.01) confirm statistically significant rhythmicity for both genes in all tissues. ( C ) Per2 and Esr1 circadian rhythms are abolished in Per1 −/− / Per2 −/− double knockout mice. Liver expression data from wild-type and Per1/2 dKO mice ( GSE171975 ) show that in wild-type liver, both Per2 and Esr1 exhibit robust circadian oscillations (period ∼23 h, p < 0.01). In contrast, both genes completely lose rhythmicity in Per1/2 dKO liver tissue, with expression remaining flat across all time points. Importantly, basal transcript levels are maintained despite loss of oscillation, demonstrating that Esr1 transcription per se does not require functional PER proteins, but rather that circadian modulation of expression requires clock function. ( D ) Pou2f1 and Brca1 transcripts show no circadian rhythmicity at the mRNA level. Upper panel: Pou2f1 expression remains relatively constant across the circadian cycle in both wild-type and Per1/2 dKO liver, with no statistically significant oscillations. Lower panel: Brca1 expression similarly lacks circadian rhythmicity in both genotypes. These non-rhythmic expression patterns contrast sharply with the robust oscillations observed for Per2 and Esr1 , suggesting that constitutively expressed POU2F1(OCT-1) and BRCA1 serve as stable scaffolding factors that cooperate with rhythmically expressed PER2 to impose circadian control on Esr1 transcription. ( E ) Meta2d analysis results for Brca1 and Pou2f1 showing circadian parameters and statistical assessment. p-values confirm the absence of significant circadian rhythmicity (p > 0.01) for both genes in both wild-type and Per1/2 dKO animals. ( F ) Direct temporal comparison of Per2 and Esr1 oscillations in wild-type and Per1/2 dKO liver. Per2 (red) and Esr1 (blue) expression from GSE171975 are plotted together to visualize their temporal relationship.
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PER2 integrates circadian and transcriptional signals at the mouse Esr1 promoter. ( A ) Time-course expression profiles of Esr1 and Per2 mRNA showing circadian oscillations in multiple mouse tissues. Wild-type mice were entrained to 12-h light:12-h dark cycles for one week, then released into constant darkness. Tissues (white adipose tissue, liver, and kidney) were collected at 2 h intervals for 48 h mRNA expression levels (normalized counts) are plotted against circadian time (CT). Fitted cosine curves (blue for Esr1 , red for Per2 ) show that both genes oscillate with similar periodicity across tissues, with tissue-specific phase relationships. ( B ) Quantitative circadian parameters (period, phase, amplitude, and baseline expression) determined by meta2d analysis of data shown in panel A. Upper table. Circadian periods for Esr1 and Per2 in each tissue show remarkable similarity (white adipose: ∼24.2 h for both; liver: ∼23.8 h Esr1 , ∼23.5 h Per2 ; kidney: ∼24.1 h for both). Lower table. Phase analysis reveals tissue-specific phase relationships: Esr1 leads Per2 by 2–4 h in white adipose tissue and kidney, while lagging by ∼1–2 h in liver. P-values (p < 0.01) confirm statistically significant rhythmicity for both genes in all tissues. ( C ) Per2 and Esr1 circadian rhythms are abolished in Per1 −/− / Per2 −/− double knockout mice. Liver expression data from wild-type and Per1/2 dKO mice ( GSE171975 ) show that in wild-type liver, both Per2 and Esr1 exhibit robust circadian oscillations (period ∼23 h, p < 0.01). In contrast, both genes completely lose rhythmicity in Per1/2 dKO liver tissue, with expression remaining flat across all time points. Importantly, basal transcript levels are maintained despite loss of oscillation, demonstrating that Esr1 transcription per se does not require functional PER proteins, but rather that circadian modulation of expression requires clock function. ( D ) Pou2f1 and Brca1 transcripts show no circadian rhythmicity at the mRNA level. Upper panel: Pou2f1 expression remains relatively constant across the circadian cycle in both wild-type and Per1/2 dKO liver, with no statistically significant oscillations. Lower panel: Brca1 expression similarly lacks circadian rhythmicity in both genotypes. These non-rhythmic expression patterns contrast sharply with the robust oscillations observed for Per2 and Esr1 , suggesting that constitutively expressed POU2F1(OCT-1) and BRCA1 serve as stable scaffolding factors that cooperate with rhythmically expressed PER2 to impose circadian control on Esr1 transcription. ( E ) Meta2d analysis results for Brca1 and Pou2f1 showing circadian parameters and statistical assessment. p-values confirm the absence of significant circadian rhythmicity (p > 0.01) for both genes in both wild-type and Per1/2 dKO animals. ( F ) Direct temporal comparison of Per2 and Esr1 oscillations in wild-type and Per1/2 dKO liver. Per2 (red) and Esr1 (blue) expression from GSE171975 are plotted together to visualize their temporal relationship.

Journal: Neurobiology of Sleep and Circadian Rhythms

Article Title: The PER2:BRCA1:POU2F1(OCT-1) ternary complex represents a multi-component scaffold model for circadian gene regulation

doi: 10.1016/j.nbscr.2025.100141

Figure Lengend Snippet: PER2 integrates circadian and transcriptional signals at the mouse Esr1 promoter. ( A ) Time-course expression profiles of Esr1 and Per2 mRNA showing circadian oscillations in multiple mouse tissues. Wild-type mice were entrained to 12-h light:12-h dark cycles for one week, then released into constant darkness. Tissues (white adipose tissue, liver, and kidney) were collected at 2 h intervals for 48 h mRNA expression levels (normalized counts) are plotted against circadian time (CT). Fitted cosine curves (blue for Esr1 , red for Per2 ) show that both genes oscillate with similar periodicity across tissues, with tissue-specific phase relationships. ( B ) Quantitative circadian parameters (period, phase, amplitude, and baseline expression) determined by meta2d analysis of data shown in panel A. Upper table. Circadian periods for Esr1 and Per2 in each tissue show remarkable similarity (white adipose: ∼24.2 h for both; liver: ∼23.8 h Esr1 , ∼23.5 h Per2 ; kidney: ∼24.1 h for both). Lower table. Phase analysis reveals tissue-specific phase relationships: Esr1 leads Per2 by 2–4 h in white adipose tissue and kidney, while lagging by ∼1–2 h in liver. P-values (p < 0.01) confirm statistically significant rhythmicity for both genes in all tissues. ( C ) Per2 and Esr1 circadian rhythms are abolished in Per1 −/− / Per2 −/− double knockout mice. Liver expression data from wild-type and Per1/2 dKO mice ( GSE171975 ) show that in wild-type liver, both Per2 and Esr1 exhibit robust circadian oscillations (period ∼23 h, p < 0.01). In contrast, both genes completely lose rhythmicity in Per1/2 dKO liver tissue, with expression remaining flat across all time points. Importantly, basal transcript levels are maintained despite loss of oscillation, demonstrating that Esr1 transcription per se does not require functional PER proteins, but rather that circadian modulation of expression requires clock function. ( D ) Pou2f1 and Brca1 transcripts show no circadian rhythmicity at the mRNA level. Upper panel: Pou2f1 expression remains relatively constant across the circadian cycle in both wild-type and Per1/2 dKO liver, with no statistically significant oscillations. Lower panel: Brca1 expression similarly lacks circadian rhythmicity in both genotypes. These non-rhythmic expression patterns contrast sharply with the robust oscillations observed for Per2 and Esr1 , suggesting that constitutively expressed POU2F1(OCT-1) and BRCA1 serve as stable scaffolding factors that cooperate with rhythmically expressed PER2 to impose circadian control on Esr1 transcription. ( E ) Meta2d analysis results for Brca1 and Pou2f1 showing circadian parameters and statistical assessment. p-values confirm the absence of significant circadian rhythmicity (p > 0.01) for both genes in both wild-type and Per1/2 dKO animals. ( F ) Direct temporal comparison of Per2 and Esr1 oscillations in wild-type and Per1/2 dKO liver. Per2 (red) and Esr1 (blue) expression from GSE171975 are plotted together to visualize their temporal relationship.

Article Snippet: Circadian gene expression datasets were obtained from the National Center for Biotechnology Information (NCBI) Gene Expression Omnibus (GEO) database.

Techniques: Expressing, Double Knockout, Functional Assay, Scaffolding, Control, Comparison