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Proteins pulled down by CREB, part 2

ABSTRACT: Hepatocarcinoma is the third leading cause of death in cancer in the world. In recent years, research on CREB in hepatocellular carcinoma has become a hotspot, so our research group wants to use the mass spectrometry analysis what proteins can bind with CREB, and then explore the links between CREB and hepatocellular carcinoma.

INSTRUMENT(S): maXis

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Hepatocyte, Cell Culture

SUBMITTER: hui du

LAB HEAD: hui du

PROVIDER: PXD008261 | Pride | 2019-11-08

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	281474976715380.mgf	Mgf
	281474976715380.pride.mgf.gz	Mgf
	F009800-HA-2.mzid.gz	Mzid
	analysis.baf	Other

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1 - 4 of 4

Publications

ILF2 Directly Binds and Stabilizes CREB to Stimulate Malignant Phenotypes of Liver Cancer Cells.

Du Hui H Le Yun Y Sun Fenyong F Li Kai K Xu Yanfeng Y

Analytical cellular pathology (Amsterdam) 20190210

Cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB) is overexpressed and has an oncogenic role in hepatocellular carcinoma (HCC). Interleukin enhancer binding factor 2 (ILF2) has become research hotspot in liver cancer recently. However, it is still unclear whether and how CREB and ILF2 interact with each other. And how this interaction exerts its role in occurrence and development of liver cancer is still unclear. Here, we found that ILF2 directly bound with CREB, and ...[more]

PMID: 30881868

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CCT3 acts as upstream of YAP and TFCP2 to be a potential target and tumor biomarker in liver cancer

Project description:Recently, we've reported that pro-tumorigenic roles of YAP in liver cancer are indispensable of TFCP2 act as upstream to simultaneously control YAP.The aim of this study is to uncover such proteins and evaluate whether the candidates are potential YAP-associated therapeutic target and diagnostic marker Via mass spectrometry, CCT3 was identified to co-interact with YAP and TFCP2, and importantly.

2019-09-11 | PXD013143 | Pride

Effect of circPTPRM on the biological behaviors of hepatocellular carcinoma cells in vitro and its clinical significance.

Project description:In this paper, a new circRNA was discovered by RNA sequencing, and its relationship with hepatocarcinoma proliferation, apoptosis, invasion and migration and clinical correlation of hepatocellular carcinoma were verified from different angles, providing a basis for further discussion on the mechanism of promoting the occurrence and development of hepatocellular carcinoma.

2019-09-17 | GSE125469 | GEO

AMPK and calcineurin induced longevity is mediated by CRTC-1 and CREB

Project description:AMPK (AAK-2) and calcineurin (TAX-6) mediate longevity exclusively through post-translational modification of CRTC-1, the sole C. elegans CRTC (CREB regulated transcriptional coactivator). We performed microarrays to examine the transcriptional responses elicited by the pro-longevity: activation of AMPK, deactivation of calcineurin, and decrease of CREB (CRH-1) activity. Gene expression profiles for crh1 (nn3315) and tax-6 (ok2065) mutants, aak-2c (aa1-321) overexpressers and WT (N2) controls were obtained by measuring RNA levels in replicate pools of 3000 synchronized L4 worms. Three replicate pools of each strain were prepared on separate days.

2010-11-20 | E-GEOD-25513 | biostudies-arrayexpress

Hepatic Gene Expression Induced by CREB-H-ΔTC

Project description:The cAMP-response element binding protein H (CREB-H) is a transcription factor expressed in liver and intestinal tissues. It is well known for regulating many lipid and glucose metabolism genes. Our group aimed to screen for additional or potential genes that may be downstream of CREB-H transcription. To prevent inaccuracy arisen from endogenous CREB-H expression, we used CREB-H-knockout (CREB-H KO) mice for this study.

2024-10-26 | GSE246514 | GEO

HIV-1 gp120 impairs spatial memory through CREB

Project description:HIV-associated neurocognitive disorders (HAND) remain an unsolved problem that persists despite using antiretroviral therapy. We have obtained data showing that HIV-gp120 protein contributes to neurodegeneration through metabolic reprogramming. This led to decreased ATP levels, lower mitochondrial DNA copy numbers, and loss of mitochondria cristae, all-important for mitochondrial biogenesis. gp120 protein also disrupted mitochondrial movement and synaptic plasticity. Searching for the mechanisms involved, we found that gp120 alters the cyclic AMP response element-binding protein (CREB) phosphorylation on serine residue 133 necessary for its function as a transcription factor. Since CREB regulates the promoters of PGC1 and BDNF genes, we found that CREB dephosphorylation causes PGC1 and BDNF loss of functions. Our data was validated in vitro and in vivo. The negative effect of gp120 was alleviated in cells and animals in the presence of rolipram that inhibits the phosphodiesterase protein 4 (PDE4) and restores CREB phosphorylation. We concluded that HIV-gp120 protein contributes to HAND via inhibition of CREB protein function.

2022-06-09 | PXD031891 | Pride

Transcription Profiling of CREB-H

Project description:The aim is to identify transcripts which are differentially regulated upon the duxycline-controlled induction of a transcription factor, CREB-H.<br>A cell line was developed 293.CREB-H which contains this factor under th etight control of a doxycline rwgukated activator suhc that after doxycline treatment, CREB-H is induced, and then this factor will act upon cellular target genes. These will be identiifed by comparing the profile in th esame cells before and after doxycline treatment<br>

2010-12-09 | E-MEXP-3004 | biostudies-arrayexpress

Expression Profile of CREB knockdown in Myeloid Leukemia Cells

Project description:Background. The cAMP Response Element Binding Protein, CREB, is a transcription factor that regulates cell proliferation, differentiation, and survival in several model systems, including neuronal and hematopoietic cells. We demonstrated that CREB is overexpressed in acute myeloid and leukemia cells compared to normal hematopoietic stem cells. CREB knockdown inhibits leukemic cell proliferation in vitro and in vivo, but does not affect long-term hematopoietic reconstitution. Therefore, we propose CREB to be a potential target for therapy. To understand downstream pathways regulating CREB, we performed expression profiling with RNA from the K562 myeloid leukemia cell line. Results. By combining our expression data from CREB knockdown cells with prior ChIP data on CREB binding we were able to identify a list of putative CREB regulated genes. We performed extensive analyses on the top genes in this list as high confidence CREB targets. We found that this list is enriched for genes involved in cancer, and unexpectedly, highly enriched for histone genes. Furthermore, histone genes regulated by CREB were more likely to be specifically expressed in hematopoietic lineages. The transcription factor Elk-1 was upregulated in response to CREB deletion. Conclusions. We have identified a high confidence list of CREB targets in K562 cells. These genes allow us to begin to understand the mechanisms by which CREB contributes to acute leukemia. In particular, we speculate that the regulation of histone genes may play an important role in this process, by possibly altering the regulation of DNA replication during the cell cycle.

2008-08-30 | GSE12056 | GEO

Characterize CREB target genes in different tissue types

Project description:The CREB family of transcription factors stimulates cellular gene expression following phosphorylation at a conserved serine (Ser133 in CREB1) in response to cAMP and other extracellular signals. In order to characterize CREB target genes in various tissues, we give a cAMP agonist, forskolin (FSK), to cell lines or primary cultures and monitor the gene expression. To eliminate CREB-independent effects of FSK on cellular gene expression, we employed a dominant negative form of CREB called A-CREB, which dimerizes selectively with and blocks the DNA binding activity of CREB but not other bZIP family members. Therefore, genes that are induced by cAMP and the induction was blocked by A-CREB treatment likely represents CREB target genes. Notes: 1) In HEK293T cells, besides the Control+FSK+(FSK-ACREB) experiments, a different set of experiments showing FSK effect on 1hr and 4hr is included. The two sets of data in HEK293T were generated at different times with different batch of cells, and comparison should be limited within each set. The cAMP induced genes at 1hr, however, was similar between the two sets. 2) These is no ACREB data for pancreatic islets or hepatocytes. For hepatocytes, however, we have included fasting liver and refed liver in additional to FSK treated primary hepatocytes. During fasting, glucagon induces cAMP increase in the liver and CREB is activated. Therefore, a more reliable list of CREB target genes in hepatocytes can be obtained by selecting those genes are that induced both during fasting and in FSK treated primary culture. Keywords: parallel sample

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Transcription profiling of mouse transgenics expressing A-CREB to investigate basal and kainate-induced gene expression in A-CREB mouse hippocampi

Project description:The cAMP responsive element binding protein (CREB) pathway has been involved in two major cascades of gene expression regulating neuronal function. The first one presents CREB as a critical component of the molecular switch that control longlasting forms of neuronal plasticity and learning. The second one relates CREB to neuronal survival and protection. To investigate the role of CREB-dependent gene expression in neuronal plasticity and survival in vivo, we generated bitransgenic mice expressing A-CREB, an artificial peptide with strong and broad inhibitory effect on the CREB family, in forebrain neurons in a regulatable manner. The expression of ACREB in hippocampal neurons impaired L-LTP, reduced intrinsic excitability and the susceptibility to induced seizures, and altered both basal and activity-driven gene expression. In the long-term, the chronic inhibition of CREB function caused severe loss of neurons in the CA1 subfield as well as in other brain regions. Our experiments confirmed previous findings in CREB deficient mutants and revealed new aspects of CREB-dependent gene expression in the hippocampus supporting a dual role for CREB-dependent gene expression regulating intrinsic and synaptic plasticity and promoting neuronal survival. manufacturer's protocol. Experiment Overall Design: Each sample contained total RNA from the hippocampi of a group of 3-4 three weeks old mice. We obtained duplicate samples for each experimental condition (in total 14 WT and 20 A-CREB mice where used in this experiment). Mouse Genome 430 2.0 genechips were hybridized, stained, washed and screened for quality according to the manufacturer's protocol.

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Project description:Treatments that stimulate neuronal excitability enhance motor performance after stroke.cAMP-response-element binding protein (CREB) is a transcription factor that plays a key rolein neuronal excitability. Increasing the levels of CREB with a viral vector in a small pool ofmotor neurons enhances motor recovery after stroke, while blocking CREB signaling preventsstroke recovery. Silencing CREB-transfected neurons in the peri-infarct region with thehM4di-DREADD blocks motor recovery. Reversing this inhibition allows recovery to continue,demonstrating that it is possible to turn off and on stroke recovery by manipulating theactivity of CREB-transfected neurons. CREB transfection enhances re-mapping of injuredsomatosensory and motor circuits, and induces the formation of new connections withinthese circuits. CREB is a central molecular node in the circuit responses after stroke that leadto recovery from motor deficits.

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