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A Novel Method for Visualizing In-Vivo Rates of Protein Degradation Provides Insight into how TRIM28 Regulates Muscle Size

ABSTRACT: A Novel Method for Visualizing In-Vivo Rates of Protein Degradation Provides Insight into how TRIM28 Regulates Muscle Size

PROVIDER: PRJNA989589 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25099160_1.fastq.gz	Fastqsanger.gz
	SRR25099160_2.fastq.gz	Fastqsanger.gz
	SRR25099161_1.fastq.gz	Fastqsanger.gz
	SRR25099161_2.fastq.gz	Fastqsanger.gz
	SRR25099162_1.fastq.gz	Fastqsanger.gz

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A Novel Method for Visualizing In-Vivo Rates of Protein Degradation Provides Insight into how TRIM28 Regulates Muscle Size

Project description:Skeletal muscle size is controlled by the balance between protein synthesis and protein degradation. Given the essential role of skeletal muscle in maintaining a high quality of life, understanding the mechanisms that modulate this balance are of critical importance. Previously, we demonstrated that muscle-specific knockout of TRIM28 reduces muscle size and function, and in the current study, we discovered that this effect is associated with an increase in protein degradation and a dramatic reduction in the expression of Mettl21c. Importantly, we also determined that overexpression of Mettl21c is sufficient to induce hypertrophy in both control TRIM28 knockout muscles. Moreover, we developed a simple pulse-chase biorthogonal non-canonical amino acid tagging technique that enabled us to visualize the in-vivo rate of protein degradation, and with this technique were able to conclude that the hypertrophic effect of Mettl21c is due, at least in part, to an inhibition of protein degradation.

2023-06-30 | GSE236262 | GEO

A novel method for visualizing <i>in-vivo</i> rates of protein degradation provides insight into how TRIM28 regulates muscle size.

Project description:Skeletal muscle size is controlled by the balance between protein synthesis and protein degradation. Given the essential role of skeletal muscle in maintaining a high quality of life, understanding the mechanisms that modulate this balance are of critical importance. Previously, we demonstrated that muscle-specific knockout of TRIM28 reduces muscle size and function and in the current study, we discovered that this effect is associated with an increase in protein degradation and a dramatic reduction in the expression of Mettl21c. Importantly, we also determined that overexpression of Mettl21c is sufficient to induce hypertrophy in both control and TRIM28 knockout muscles. Moreover, we developed a simple pulse-chase biorthogonal non-canonical amino acid tagging technique that enabled us to visualize the in vivo rate of protein degradation, and with this technique were able to conclude that the hypertrophic effect of Mettl21c is due, at least in part, to an inhibition of protein degradation.

| S-EPMC10105291 | biostudies-literature

TRIM28 is essential for erythroblast differentiation in the mouse

Project description:We discovered that Trim28 genetic loss in the adult mouse leads to defective immature erythropoiesis in the bone marrow and consequently to anemia.We further found that TRIM28 controls erythropoiesis in a cell-autonomous manner by inducibly deleting Trim28 exclusively in hematopoietic cells. Finally, in the absence of TRIM28 we observed increased apoptosis as well as diminished expression of multiple erythroid transcription factors and heme biosynthetic enzymes in immature erythroid cells. Thus, TRIM28 is essential for the cell-autonomous development of immature erythroblasts in the bone marrow. To induce Cre recombinase from the Mx1Cre transgene, poly(I:C) was injected 5 times every other day. Mice were analyzed two weeks after completion of poly(I:C) administration. TRIM28 mutant mice generate two distinct types of immature erythroid cells; KOa, with 5-8% of the Trim28 gene remaining undeleted (still bearing 26% of residual mRNA), and KOb, with 1-4% of the gene remaining undeleted (and with 18% of mRNA remaining).

2013-10-04 | E-GEOD-49843 | biostudies-arrayexpress

RNA-seq of gonadal adipose tissue from male and female Trim28-WT and Trim28 adipose specific KO mice

Project description:Many genes have been implicated in WAT lipid metabolism, including tripartite motif containing 28 (Trim28), a gene proposed to primarily influence adiposity via epigenetic mechanisms in embryonic development. We set out to determine if adipose specific deletion of Trim28 led to changes in adipose tissue function and molecular phenotype. We performed transcriptomics analysis on adipose tissue taken from WT and adipose specific Trim28 KO mice to investigate their molecular phenotype, and to identify pathways altered in KO animals.

2020-11-25 | E-MTAB-9809 | biostudies-arrayexpress

TRIM28 silences endogenous retroviruses in neural progenitor cells

Project description:Here we show that in neural progenitor cells (NPCs) TRIM28 silences transcription of two groups of endogenous retroviruses (ERVs): IAP1 and MMERVK10C. Derepression of ERVs in Trim28-deficient NPCs was associated with a loss of H3K9me3 and resulted in transcriptional upregulation and reverse transcription. These findings demonstrate a unique dynamic transcriptional regulation of ERVs in NPCs. Analysis of upregulation of ERVs in Trim28-deficient NPCs

2015-01-07 | E-GEOD-45930 | biostudies-arrayexpress

TRIM28 regulates RNA polymerase II promoter proximal pausing and entry into processive elongation

Project description:Analysis of total PolII and Ser2-phosphorylated PolII genomic occupancy in control-transfected (WT) or Trim28-knockdown (Trim28-KD) embryonic stem cells. Embryonic stem cells were transfected with luciferase siRNA (WT) or Trim28 siRNA (Trim28 KD) in duplicate experiments. 48 hrs after transfection, cells were crosslinked with formaldehyde, collected, lysed, and chromatin was fragmented with sonication. Total PolII or Ser2-phosphorylated PolII genomic occupancy in WT or Trim28 KD cells were determined by ChIP-seq.

2014-07-28 | E-GEOD-48253 | biostudies-arrayexpress

WTX interacts with the transcriptional regulator TRIM28 to mediate cellular differentiation

Project description:WTX encodes a tumor suppressor implicated in Wilms tumor and in mesenchymal differentiation, with distinct functions in the cytoplasm, at the plasma membrane and in the nucleus. Here we report that the transcriptional corepressor TRIM28 is the major binding partner for nuclear WTX. The WTX-TRIM28 interaction supports chromatin binding by TRIM28, enhancing transcriptional silencing of some TRIM28 target sequences. In mouse ES cells, where TRIM28-mediated silencing of repetitive sequences is best characterized, Wtx knockdown similarly derepresses endogenous retroviruses and LINE elements. We performed digital gene expression (DGE) profiling using Helicos RNA sequencing. Helicos sequencing does not involve an amplification step, hence it has less bias, especially in sequencing of repetitive elements. We sequenced RNA extracted from mouse ESCs harboring GFP, Wtx or Trim28 hairpins. The resulting sequence reads were aligned with the RefSeq database as well as Repbase, which is a database for the repetitive sequences.

2015-04-16 | E-GEOD-60418 | biostudies-arrayexpress

TRIM28 modulates nuclear receptor signaling to regulate uterine function

Project description:This project identified that TRIM28 can modulate progesterone and estrogen signaling in both human and mouse endometrium to regulate its normal functions during pregnancy. TRIM28 showed proximal localization and co-immunoprecipitation with PR and ERalpha. The ablation of TRIM28 can inhibit the chromatin binding activity of PR and ERalpha leading to disrupted estrogen and progesterone signaling. This immunoprecipitation using TRIM28 antibody was performed in pre-decidual human endometrial stromal cells (HESCs) without any hormone treatment. The potential interacting proteins of TRIM28 was analyzed using mass spec.

2023-07-05 | MSV000092346 | MassIVE

Visualizing programmed lineage trajectories at cancer initiation

Project description:Visualizing programmed lineage trajectories at cancer initiation

| PRJNA639282 | ENA

Transcriptome data after TRIM28 knockdown in A375 melanoma cells

Project description:TRIM28 is a bromodomain protein implicated in the regulation of tumor growth. TRIM28 regulates gene expression by recruiting epigenetic writers including HDACs, SETDB1 and HP1. To determine the role of TRIM28 in melanoma cells we knocked down TRIM28 using lentiviral shRNA constructs followed by gene expression analysis using HTA 2.0 GeneChip.

2019-06-21 | GSE133073 | GEO

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