LIVIVO - Search results -

Search results

Result 1 - 10 of total 148

Search options

Article ; Online: PERK promotes immunosuppressive M2 macrophage phenotype by metabolic reprogramming and epigenetic modifications through the PERK-ATF4-PSAT1 axis.

Pratap, Uday P / Vadlamudi, Ratna K

Immunometabolism (Cobham (Surrey, England))

2022 Volume 4, Issue 3, Page(s) e00007

Abstract: The endoplasmic reticulum (ER) is a specialized organelle that participates in multiple cellular functions including protein folding, maturation, trafficking, and degradation to maintain homeostasis. However, hostile conditions in the tumor ... ...

Abstract	The endoplasmic reticulum (ER) is a specialized organelle that participates in multiple cellular functions including protein folding, maturation, trafficking, and degradation to maintain homeostasis. However, hostile conditions in the tumor microenvironment (TME) disturb ER homeostasis. To overcome these conditions, cells activate ER stress response pathways, which are shown to augment the suppressive phenotypes of immune cells; however, the molecular mechanisms underpinning this process remain elusive. Here, we discuss a recent study by Raines et al, that suggests the role of the helper T-cell 2 (TH2) cytokine interleukin-4 (IL-4), and the TME in facilitating a protein kinase RNA-like ER kinase (PERK)-signaling cascade in macrophages, which promotes immunosuppressive M2 macrophage activation and proliferation. Further, the authors showed that PERK signaling promotes both mitochondrial respirations to fulfill cellular energy requirements and signaling through ATF4, which regulate phosphoserine aminotransferase 1 (PSAT1) activity to mediate the serine biosynthesis pathway. These results highlight a previously uncharacterized role for PERK in cellular metabolism and epigenetic modification in M2 macrophages, and thus offers a new therapeutic strategy for overcoming the immunosuppressive effects in the TME.
Language	English
Publishing date	2022-07-29
Publishing country	England
Document type	Journal Article
ISSN	2633-0407
ISSN (online)	2633-0407
DOI	10.1097/IN9.0000000000000007
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Role of estrogen receptor coregulators in endocrine resistant breast cancer.

Altwegg, Kristin A / Vadlamudi, Ratna K

Exploration of targeted anti-tumor therapy

2021 Volume 2, Page(s) 385–400

Abstract: Breast cancer (BC) is the most ubiquitous cancer in women. Approximately 70-80% of BC diagnoses are positive for estrogen receptor (ER) alpha (ERα). The steroid hormone estrogen [17β-estradiol (E2)] plays a vital role both in the initiation and ... ...

Abstract	Breast cancer (BC) is the most ubiquitous cancer in women. Approximately 70-80% of BC diagnoses are positive for estrogen receptor (ER) alpha (ERα). The steroid hormone estrogen [17β-estradiol (E2)] plays a vital role both in the initiation and progression of BC. The E2-ERα mediated actions involve genomic signaling and non-genomic signaling. The specificity and magnitude of ERα signaling are mediated by interactions between ERα and several coregulator proteins called coactivators or corepressors. Alterations in the levels of coregulators are common during BC progression and they enhance ligand-dependent and ligand-independent ERα signaling which drives BC growth, progression, and endocrine therapy resistance. Many ERα coregulator proteins function as scaffolding proteins and some have intrinsic or associated enzymatic activities, thus the targeting of coregulators for blocking BC progression is a challenging task. Emerging data from
Language	English
Publishing date	2021-08-30
Publishing country	United States
Document type	Journal Article
ISSN	2692-3114
ISSN (online)	2692-3114
DOI	10.37349/etat.2021.00052
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Programmed death ligand 1 signals in cancer cells.

Kornepati, Anand V R / Vadlamudi, Ratna K / Curiel, Tyler J

Nature reviews. Cancer

2022 Volume 22, Issue 3, Page(s) 174–189

Abstract: The paradigm of surface-expressed programmed death ligand 1 (PDL1) signalling to immune cell programmed death 1 (PD1) to inhibit antitumour immunity has helped to develop effective and revolutionary immunotherapies using antibodies blocking these cell- ... ...

Abstract	The paradigm of surface-expressed programmed death ligand 1 (PDL1) signalling to immune cell programmed death 1 (PD1) to inhibit antitumour immunity has helped to develop effective and revolutionary immunotherapies using antibodies blocking these cell-extrinsic interactions. The recent discovery of cancer cell-intrinsic PDL1 signals has broadened understanding of pathologic tumour PDL1 signal consequences that now includes control of tumour growth and survival pathways, stemness, immune effects, DNA damage responses and gene expression regulation. Many such effects are PD1-independent. These insights demonstrate that the prevailing cell-extrinsic PDL1 signalling paradigm is useful, but incomplete in important respects. This Perspective discusses historical and recent advances in understanding cancer cell-intrinsic PDL1 signals, mechanisms for signal controls and important immunopathologic consequences including resistance to cytotoxic agents, targeted small molecules and immunotherapies. Cancer cell-intrinsic PDL1 signals present novel drug discovery targets and also have potential as reliable treatment response biomarkers. Cancer cell-intrinsic PD1 signals and cell-intrinsic PDL1 signals in non-cancer cells are discussed briefly, as are PDL1 signals from soluble and vesicle-bound PDL1 and PDL1 isoforms. We conclude with suggestions for addressing the most pressing challenges and opportunities in this rapidly developing field.
MeSH term(s)	B7-H1 Antigen ; Drug Discovery ; Humans ; Immunotherapy ; Neoplasms/therapy
Chemical Substances	B7-H1 Antigen
Language	English
Publishing date	2022-01-14
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2062767-1
ISSN	1474-1768 ; 1474-175X
ISSN (online)	1474-1768
ISSN	1474-175X
DOI	10.1038/s41568-021-00431-4
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 5563: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 24: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Publisher Correction: Programmed death ligand 1 signals in cancer cells.

Kornepati, Anand V R / Vadlamudi, Ratna K / Curiel, Tyler J

Nature reviews. Cancer

2022 Volume 22, Issue 3, Page(s) 190

Language	English
Publishing date	2022-01-18
Publishing country	England
Document type	Published Erratum
ZDB-ID	2062767-1
ISSN	1474-1768 ; 1474-175X
ISSN (online)	1474-1768
ISSN	1474-175X
DOI	10.1038/s41568-022-00445-6
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 5563: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 24: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Development and Characterization of Inducible Astrocyte-Specific Aromatase Knockout Mice.

Wang, Jing / Pratap, Uday P / Lu, Yujiao / Sareddy, Gangadhara R / Tekmal, Rajeshwar R / Vadlamudi, Ratna K / Brann, Darrell W

Biology

2023 Volume 12, Issue 4

Abstract: 17β-estradiol (E2) is produced in the brain as a neurosteroid, in addition to being an endocrine signal in the periphery. The current animal models for studying brain-derived ... ...

Abstract	17β-estradiol (E2) is produced in the brain as a neurosteroid, in addition to being an endocrine signal in the periphery. The current animal models for studying brain-derived E
Language	English
Publishing date	2023-04-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology12040621
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Development and Characterization of Inducible Astrocyte-Specific Aromatase Knockout Mice

Wang, Jing / Pratap, Uday P. / Lu, Yujiao / Sareddy, Gangadhara R. / Tekmal, Rajeshwar R. / Vadlamudi, Ratna K. / Brann, Darrell W.

Biology (Basel). 2023 Apr. 19, v. 12, no. 4

2023

Abstract: 17β-estradiol (E2) is produced in the brain as a neurosteroid, in addition to being an endocrine signal in the periphery. The current animal models for studying brain-derived E₂ include global and conditional non-inducible knockout mouse models. The aim ... ...

Abstract	17β-estradiol (E2) is produced in the brain as a neurosteroid, in addition to being an endocrine signal in the periphery. The current animal models for studying brain-derived E₂ include global and conditional non-inducible knockout mouse models. The aim of this study was to develop a tamoxifen (TMX)-inducible astrocyte-specific aromatase knockout mouse line (GFAP-ARO-iKO mice) to specifically deplete the E₂ synthesis enzymes and aromatase in astrocytes after their development in adult mice. The characterization of the GFAP-ARO-iKO mice revealed a specific and robust depletion in the aromatase expressions of their astrocytes and a significant decrease in their hippocampal E₂ levels after a GCI. The GFAP-ARO-iKO animals were alive and fertile and had a normal general brain anatomy, with a normal astrocyte shape, intensity, and distribution. In the hippocampus, after a GCI, the GFAP-ARO-iKO animals showed a major deficiency in their reactive astrogliosis, a dramatically increased neuronal loss, and increased microglial activation. These findings indicate that astrocyte-derived E₂ (ADE₂) regulates the ischemic induction of reactive astrogliosis and microglial activation and is neuroprotective in the ischemic brain. The GFAP-ARO-iKO mouse models thus provide an important new model to help elucidate the roles and functions of ADE₂ in the brain.
Keywords	adults ; aromatase ; astrocytes ; hippocampus ; knockout mutants ; mice ; models ; neurons ; tamoxifen
Language	English
Dates of publication	2023-0419
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article ; Online
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology12040621
Database	NAL-Catalogue (AGRICOLA)

Order via subito

Article ; Online: PELP1: Structure, biological function and clinical significance.

Sareddy, Gangadhara Reddy / Vadlamudi, Ratna K

Gene

2016 Volume 585, Issue 1, Page(s) 128–134

Abstract: Proline-, glutamic acid-, and leucine-rich protein 1 (PELP1) is a scaffolding protein that functions as a coregulator of several transcription factors and nuclear receptors. Notably, the PELP1 protein has a histone-binding domain, recognizes histone ... ...

Abstract	Proline-, glutamic acid-, and leucine-rich protein 1 (PELP1) is a scaffolding protein that functions as a coregulator of several transcription factors and nuclear receptors. Notably, the PELP1 protein has a histone-binding domain, recognizes histone modifications and interacts with several chromatin-modifying complexes. PELP1 serves as a substrate of multitude of kinases, and phosphorylation regulates its functions in various complexes. Further, PELP1 plays essential roles in several pathways including hormonal signaling, cell cycle progression, ribosomal biogenesis, and the DNA damage response. PELP1 expression is upregulated in several cancers, its deregulation contributes to therapy resistance, and it is a prognostic biomarker for breast cancer survival. Recent evidence suggests that PELP1 represents a novel therapeutic target for many hormonal cancers. In this review, we summarized the emerging biological properties and functions of PELP1.
MeSH term(s)	Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Cell Cycle Checkpoints/genetics ; Co-Repressor Proteins/genetics ; Co-Repressor Proteins/metabolism ; DNA Repair/genetics ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Phosphorylation ; Protein Processing, Post-Translational/physiology ; Protein Structure, Tertiary ; Receptors, Cytoplasmic and Nuclear/genetics ; Signal Transduction/genetics ; Trans-Activators/genetics ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	Co-Repressor Proteins ; PELP1 protein, human ; Receptors, Cytoplasmic and Nuclear ; Trans-Activators ; Transcription Factors
Language	English
Publishing date	2016-07-01
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	391792-7
ISSN	1879-0038 ; 0378-1119
ISSN (online)	1879-0038
ISSN	0378-1119
DOI	10.1016/j.gene.2016.03.017
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1357: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Targeting LIF/LIFR signaling in cancer.

Viswanadhapalli, Suryavathi / Dileep, Kalarickal V / Zhang, Kam Y J / Nair, Hareesh B / Vadlamudi, Ratna K

Genes & diseases

2021 Volume 9, Issue 4, Page(s) 973–980

Abstract: Leukemia inhibitory factor (LIF), and its receptor (LIFR), are commonly over-expressed in many solid cancers and recent studies have implicated LIF/LIFR axis as a promising clinical target for cancer therapy. LIF/LIFR activate oncogenic signaling ... ...

Abstract	Leukemia inhibitory factor (LIF), and its receptor (LIFR), are commonly over-expressed in many solid cancers and recent studies have implicated LIF/LIFR axis as a promising clinical target for cancer therapy. LIF/LIFR activate oncogenic signaling pathways including JAK/STAT3 as immediate effectors and MAPK, AKT, mTOR further downstream. LIF/LIFR signaling plays a key role in tumor growth, progression, metastasis, stemness and therapy resistance. Many solid cancers show overexpression of LIF and autocrine stimulation of the LIF/LIFR axis; these are associated with a poorer relapse-free survival. LIF/LIFR signaling also plays a role in modulating multiple immune cell types present in tumor micro environment (TME). Recently, two targeted agents that target LIF (humanized anti-LIF antibody, MSC-1) and LIFR inhibitor (EC359) were under development. Both agents showed effectivity in preclinical models and clinical trials using MSC-1 antibody are in progress. This article reviews the significance of LIF/LIFR pathways and inhibitors that disrupt this process for the treatment of cancer.
Language	English
Publishing date	2021-04-29
Publishing country	China
Document type	Journal Article ; Review
ZDB-ID	2821806-1
ISSN	2352-3042 ; 2352-3042
ISSN (online)	2352-3042
ISSN	2352-3042
DOI	10.1016/j.gendis.2021.04.003
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Cancer therapy using natural ligands that target estrogen receptor beta.

Sareddy, Gangadhara R / Vadlamudi, Ratna K

Chinese journal of natural medicines

2015 Volume 13, Issue 11, Page(s) 801–807

Abstract: Estrogen receptor beta (ERβ) is one of the two key receptors (ERα, ERβ) that facilitate biological actions of 17β-estradiol (E2). ERβ is widely expressed in many tissues, and its expression is reduced or lost during progression of many tumors. ERβ ... ...

Abstract	Estrogen receptor beta (ERβ) is one of the two key receptors (ERα, ERβ) that facilitate biological actions of 17β-estradiol (E2). ERβ is widely expressed in many tissues, and its expression is reduced or lost during progression of many tumors. ERβ facilitates estrogen signaling by both genomic (classical and non-classical) and extra-nuclear signaling. Emerging evidence suggests that ERβ functions as a tissue-specific tumor suppressor with anti-proliferative actions. Recent studies have identified a number of naturally available selective ERβ agonists. Targeting ERβ using its naturally available ligands is an attractive approach for treating and preventing cancers. This review presents the beneficial actions of ERβ signaling and clinical utility of several natural ERβ ligands as potential cancer therapy.
MeSH term(s)	Antineoplastic Agents, Phytogenic/pharmacology ; Antineoplastic Agents, Phytogenic/therapeutic use ; Equol/pharmacology ; Equol/therapeutic use ; Estrogen Receptor beta/antagonists & inhibitors ; Estrogen Receptor beta/metabolism ; Flavanones/pharmacology ; Flavanones/therapeutic use ; Genistein/pharmacology ; Genistein/therapeutic use ; Glycyrrhiza/chemistry ; Humans ; Ligands ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Phytotherapy ; Plant Extracts/pharmacology ; Plant Extracts/therapeutic use ; Glycine max/chemistry
Chemical Substances	Antineoplastic Agents, Phytogenic ; Estrogen Receptor beta ; Flavanones ; Ligands ; Plant Extracts ; Equol (531-95-3) ; Genistein (DH2M523P0H) ; liquiritigenin (T194LKP9W6)
Language	English
Publishing date	2015-12-22
Publishing country	China
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2192577-X
ISSN	1875-5364 ; 2095-6975 ; 1672-3651
ISSN (online)	1875-5364
ISSN	2095-6975 ; 1672-3651
DOI	10.1016/S1875-5364(15)30083-2
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 6113: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article: Global Genomic and Proteomic Analysis Identified Critical Pathways Modulated by Proto-Oncogene PELP1 in TNBC.

Liu, Zexuan / Altwegg, Kristin A / Liu, Junhao / Weintraub, Susan T / Chen, Yidong / Lai, Zhao / Sareddy, Gangadhara R / Viswanadhapalli, Suryavathi / Vadlamudi, Ratna K

Cancers

2022 Volume 14, Issue 4

Abstract: The PELP1 oncogene is commonly overexpressed in many cancers, including triple negative breast cancer (TNBC). However, the mechanisms by which PELP1 contributes to TNBC progression are not well understood. To elucidate these mechanisms, we generated ... ...

Abstract	The PELP1 oncogene is commonly overexpressed in many cancers, including triple negative breast cancer (TNBC). However, the mechanisms by which PELP1 contributes to TNBC progression are not well understood. To elucidate these mechanisms, we generated CRISPR-Cas9 mediated PELP1 knockout TNBC cell lines, and alterations in the proteome were examined using global data-independent acquisition mass spectrometry (DIA-MS). Further mechanistic studies utilized shRNA knockdown, Western blotting, and RNA-seq approaches. TCGA data sets were utilized for determining the status of PELP1 in TNBC patient tumors and for examining its correlation with ribosomal proteins. Global DIA-MS studies revealed that 127 proteins are upregulated while 220 proteins are downregulated upon PELP1-KO. Bioinformatic analyses suggested that the oncogenic activities of PELP1 involve regulation of expression of ribosomal proteins and ribosomal complexes. RNA-seq studies further suggested PELP1 modulates the functions of transcription factor c-Myc in TNBC. TCGA data confirmed PELP1 has high expression in TNBC patient tumors, and this high expression pattern correlates with c-Myc, a regulator of ribosomal proteins. Collectively, our global approach studies suggest that PELP1 contributes to TNBC progression by modulation of cell cycle, apoptosis, and ribosome biogenesis pathways.
Language	English
Publishing date	2022-02-13
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14040930
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

To top

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito