LIVIVO - Search results -

Search results

Result 1 - 10 of total 11

Search options

Book ; Thesis: Identification and characterization of novel regulatory genes of post-embryonic hematopoiesis

Hemmati, Shayda

2014

Author's details	[presented by Shayda Hemmati]
Language	English
Size	110 Bl., graph. Darst.
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Univ., Diss.--Heidelberg, 2014
Database	Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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.

Details ▾

Article ; Online: PI3-kinase deletion promotes myelodysplasia by dysregulating autophagy in hematopoietic stem cells.

Ames, Kristina / Kaur, Imit / Shi, Yang / Tong, Meng M / Sinclair, Taneisha / Hemmati, Shayda / Glushakow-Smith, Shira G / Tein, Ellen / Gurska, Lindsay / Steidl, Ulrich / Dubin, Robert / Shan, Jidong / Montagna, Cristina / Pradhan, Kith / Verma, Amit / Gritsman, Kira

Science advances

2023 Volume 9, Issue 8, Page(s) eade8222

Abstract: Myelodysplastic syndrome (MDS) is a clonal malignancy arising in hematopoietic stem cells (HSCs). The mechanisms of MDS initiation in HSCs are still poorly understood. The phosphatidylinositol 3-kinase (PI3K)/AKT pathway is frequently activated in acute ... ...

Abstract	Myelodysplastic syndrome (MDS) is a clonal malignancy arising in hematopoietic stem cells (HSCs). The mechanisms of MDS initiation in HSCs are still poorly understood. The phosphatidylinositol 3-kinase (PI3K)/AKT pathway is frequently activated in acute myeloid leukemia, but in MDS, PI3K/AKT is often down-regulated. To determine whether PI3K down-regulation can perturb HSC function, we generated a triple knockout (TKO) mouse model with
MeSH term(s)	Mice ; Animals ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Hematopoietic Stem Cells ; Myelodysplastic Syndromes/metabolism ; Myelodysplastic Syndromes/pathology ; Cell Differentiation ; Mice, Knockout
Chemical Substances	Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2023-02-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.ade8222
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.

Article: Inflammatory Signaling Pathways in Preleukemic and Leukemic Stem Cells.

Hemmati, Shayda / Haque, Tamanna / Gritsman, Kira

Frontiers in oncology

2017 Volume 7, Page(s) 265

Abstract: Hematopoietic stem cells (HSCs) are a rare subset of bone marrow cells that usually exist in a quiescent state, only entering the cell cycle to replenish the blood compartment, thereby limiting the potential for errors in replication. Inflammatory ... ...

Abstract	Hematopoietic stem cells (HSCs) are a rare subset of bone marrow cells that usually exist in a quiescent state, only entering the cell cycle to replenish the blood compartment, thereby limiting the potential for errors in replication. Inflammatory signals that are released in response to environmental stressors, such as infection, trigger active cycling of HSCs. These inflammatory signals can also directly induce HSCs to release cytokines into the bone marrow environment, promoting myeloid differentiation. After stress myelopoiesis is triggered, HSCs require intracellular signaling programs to deactivate this response and return to steady state. Prolonged or excessive exposure to inflammatory cytokines, such as in prolonged infection or in chronic rheumatologic conditions, can lead to continued HSC cycling and eventual HSC loss. This promotes bone marrow failure, and can precipitate preleukemic states or leukemia through the acquisition of genetic and epigenetic changes in HSCs. This can occur through the initiation of clonal hematopoiesis, followed by the emergence preleukemic stem cells (pre-LSCs). In this review, we describe the roles of multiple inflammatory signaling pathways in the generation of pre-LSCs and in progression to myelodysplastic syndrome (MDS), myeloproliferative neoplasms, and acute myeloid leukemia (AML). In AML, activation of some inflammatory signaling pathways can promote the cycling and differentiation of LSCs, and this can be exploited therapeutically. We also discuss the therapeutic potential of modulating inflammatory signaling for the treatment of myeloid malignancies.
Language	English
Publishing date	2017-11-13
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2017.00265
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Book ; Online ; Thesis: Identification and characterization of novel regulatory genes of post-embryonic hematopoiesis

Hemmati, Shayda [Verfasser] / Glimm, Hanno [Akademischer Betreuer]

2014

Author's details	Shayda Hemmati ; Betreuer: Hanno Glimm
Keywords	Biowissenschaften, Biologie ; Life Science, Biology
Subject code	sg570
Language	English
Publisher	Universitätsbibliothek Heidelberg
Publishing place	Heidelberg
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

Full text online

Full text

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: The balance between the intronic miR-342 and its host gene Evl determines hematopoietic cell fate decision.

Herbst, Friederike / Lang, Tonio J L / Eckert, Elias S P / Wünsche, Peer / Wurm, Alexander A / Kindinger, Tim / Laaber, Karin / Hemmati, Shayda / Hotz-Wagenblatt, Agnes / Zavidij, Oksana / Paruzynski, Anna / Lu, Junyan / von Kalle, Christof / Zenz, Thorsten / Klein, Christoph / Schmidt, Manfred / Ball, Claudia R / Glimm, Hanno

Leukemia

2021 Volume 35, Issue 10, Page(s) 2948–2963

Abstract: Protein-coding and non-coding genes like miRNAs tightly control hematopoietic differentiation programs. Although miRNAs are frequently located within introns of protein-coding genes, the molecular interplay between intronic miRNAs and their host genes is ...

Abstract	Protein-coding and non-coding genes like miRNAs tightly control hematopoietic differentiation programs. Although miRNAs are frequently located within introns of protein-coding genes, the molecular interplay between intronic miRNAs and their host genes is unclear. By genomic integration site mapping of gamma-retroviral vectors in genetically corrected peripheral blood from gene therapy patients, we identified the EVL/MIR342 gene locus as a hotspot for therapeutic vector insertions indicating its accessibility and expression in human hematopoietic stem and progenitor cells. We therefore asked if and how EVL and its intronic miRNA-342 regulate hematopoiesis. Here we demonstrate that overexpression (OE) of Evl in murine primary Lin
MeSH term(s)	Animals ; Cell Adhesion Molecules/genetics ; Cell Adhesion Molecules/metabolism ; Cell Differentiation ; Hematopoiesis ; Hematopoietic Stem Cells/cytology ; Hematopoietic Stem Cells/metabolism ; Humans ; Introns ; Mice ; MicroRNAs/genetics
Chemical Substances	Cell Adhesion Molecules ; EVL protein, human ; Evl protein, mouse ; MIRN342 microRNA, human ; MicroRNAs ; Mirn342 microRNA, mouse
Language	English
Publishing date	2021-05-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	807030-1
ISSN	1476-5551 ; 0887-6924
ISSN (online)	1476-5551
ISSN	0887-6924
DOI	10.1038/s41375-021-01267-5
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 2295: 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)

Order via subito

Details ▾

Article ; Online: PI3 kinase alpha and delta promote hematopoietic stem cell activation.

Hemmati, Shayda / Sinclair, Taneisha / Tong, Meng / Bartholdy, Boris / Okabe, Rachel O / Ames, Kristina / Ostrodka, Leanne / Haque, Tamanna / Kaur, Imit / Mills, Taylor S / Agarwal, Anupriya / Pietras, Eric M / Zhao, Jean J / Roberts, Thomas M / Gritsman, Kira

JCI insight

2019 Volume 5

Abstract: Many cytokines and chemokines that are important for hematopoiesis activate the PI3K signaling pathway. Because this pathway is frequently mutated and activated in cancer, PI3K inhibitors have been developed for the treatment of several malignancies, and ...

Abstract	Many cytokines and chemokines that are important for hematopoiesis activate the PI3K signaling pathway. Because this pathway is frequently mutated and activated in cancer, PI3K inhibitors have been developed for the treatment of several malignancies, and are now being tested in the clinic in combination with chemotherapy. However, the role of PI3K in adult hematopoietic stem cells (HSCs), particularly during hematopoietic stress, is still unclear. We previously showed that the individual PI3K catalytic isoforms P110α or P110β have dispensable roles in HSC function, suggesting redundancy between PI3K isoforms in HSCs. We now demonstrate that simultaneous deletion of P110α and P110δ in double knockout (DKO) HSCs uncovers their redundant requirement in HSC cycling after 5-fluorouracil (5-FU) chemotherapy administration. In contrast, DKO HSCs are still able to exit quiescence in response to other stress stimuli, such as LPS. We found that DKO HSCs and progenitors have impaired sensing of inflammatory signals ex vivo, and that levels of IL1-β and MIG are higher in the bone marrow after LPS than after 5-FU administration. Furthermore, exogenous in vivo administration of IL1-β can induce cell cycle entry of DKO HSCs. Our findings have important clinical implications for the use of PI3K inhibitors in combination with chemotherapy.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Bone Marrow/drug effects ; Cell Cycle ; Class I Phosphatidylinositol 3-Kinases/genetics ; Disease Models, Animal ; Enzyme Inhibitors/pharmacology ; Female ; Fluorouracil/pharmacology ; Gene Expression Regulation, Enzymologic ; Gene Knockout Techniques ; Hematopoiesis/physiology ; Hematopoietic Stem Cells/drug effects ; Hematopoietic Stem Cells/metabolism ; Lipopolysaccharides/adverse effects ; Male ; Mice, Knockout ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Protein Isoforms ; Signal Transduction/drug effects
Chemical Substances	Antineoplastic Agents ; Enzyme Inhibitors ; Lipopolysaccharides ; Protein Isoforms ; Class I Phosphatidylinositol 3-Kinases (EC 2.7.1.137) ; Pik3ca protein, mouse (EC 2.7.1.137) ; Pik3cd protein, mouse (EC 2.7.1.137) ; Fluorouracil (U3P01618RT)
Language	English
Publishing date	2019-05-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.125832
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: Indoleamine 2,3-dioxygenase (IDO) is expressed at feto-placental unit throughout mouse gestation: An immunohistochemical study.

Shayda, Hemmati / Mahmood, Jeddi-Tehrani / Ebrahim, Torkabadi / Jamileh, Ghassemi / Golnaz Ensieh, Kazemi Sefat / Parivash, Danesh / Leila, Barzegar Yarmohammadi / Mohammad Mehdi, Akhondi / Amir Hassan, Zarnani

Journal of reproduction & infertility

2013 Volume 10, Issue 3, Page(s) 177–183

Abstract: Introduction: The cells expressing Indoleamine 2, 3-dioxygenase (IDO) in feto-maternal interface mediate tryptophan catabolism, hence protect allogeneic fetus from lethal rejection by maternal immune responses. In this study, we report immuno- ... ...

Abstract	Introduction: The cells expressing Indoleamine 2, 3-dioxygenase (IDO) in feto-maternal interface mediate tryptophan catabolism, hence protect allogeneic fetus from lethal rejection by maternal immune responses. In this study, we report immuno-localization of IDO(+) cells in murine reproductive tract and placenta throughout mouse pregnancy by immunohistochemistry. Materials and methods: Syngeneic pregnant mice were examined for vaginal plug to discover about their state of pregnancy. A total of three pregnant mice were examined at each stage.The examination was further confirmed by the detection of sperm in vaginal smear. On the gestational days of 2(nd), 12(th) and 18(th), the uterus and oviduct were removed and expression of IDO was investigated in the endometrium, placenta and oviduct by immunohistochemistry. Results: Our results showed that IDO is expressed consistently in feto-maternal interface throughout pregnancy. In endometrium, expression of IDO was predominantly confined to luminal and glandular epithelial cells. Cells at junctional and labyrinth zones of placenta showed strong IDO immunoreactivity as well. Conclusion: Expression of IDO at the protein level in reproductive tract of pregnant mice during entire periods of gestation points to its potential protective role in maintenance of pregnancy. In our knowledge this is the first report of expression of IDO in feto-maternal phase during murine pregnancy.
Language	English
Publishing date	2013-06-28
Publishing country	Iran
Document type	Journal Article
ZDB-ID	2548922-7
ISSN	2251-676X ; 1735-8507 ; 2228-5482 ; 1726-7536
ISSN (online)	2251-676X ; 1735-8507
ISSN	2228-5482 ; 1726-7536
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: The effect of sortilin silencing on ovarian carcinoma cells.

Ghaemimanesh, Fatemeh / Ahmadian, Gholamreza / Talebi, Saeed / Zarnani, Amir-Hassan / Behmanesh, Mehrdad / Hemmati, Shayda / Hadavi, Reza / Jeddi-Tehrani, Mahmood / Farzi, Maryam / Akhondi, Mohammad Mehdi / Rabbani, Hodjattallah

Avicenna journal of medical biotechnology

2014 Volume 6, Issue 3, Page(s) 169–177

Abstract: Background: Our preliminary data on the protein expression of SORT1 in ovarian carcinoma tissues showed that sortilin was overexpressed in ovarian carcinoma patients and cell lines, while non-malignant ovaries expressed comparably lower amount of this ... ...

Abstract	Background: Our preliminary data on the protein expression of SORT1 in ovarian carcinoma tissues showed that sortilin was overexpressed in ovarian carcinoma patients and cell lines, while non-malignant ovaries expressed comparably lower amount of this protein. In spite of diverse ligands and also different putative functions of sortilin (NTR3), the function of overexpressed sortilin in ovarian carcinoma cells is an intriguing subject of inquiry. The aim of this study was, therefore, to investigate the functional role of sortilin in survival of ovarian carcinoma cell line. Methods: Expression of sortilin was knocked down using RNAi technology in the ovarian carcinoma cell line, Caov-4. Silencing of SORT1 expression was assessed using real-time qPCR and Western blot analyses. Apoptosis induction was evaluated using flow cytometry by considering annexin-V FITC binding. [(3)H]-thymidine incorporation assay was also used to evaluate cell proliferation capacity. Results: Real-time qPCR and Western blot analyses showed that expression of sortilin was reduced by nearly 70-80% in the siRNA transfected cells. Knocking down of sortilin expression resulted in increased apoptosis (27.5±0.48%) in siRNA-treated ovarian carcinoma cell line. Sortilin silencing led to significant inhibition of proliferation (40.1%) in siRNA-transfected Caov-4 cells as compared to mock control-transfected counterpart (p < 0.05). Conclusion: As it was suspected from overexpression of sortilin in ovarian tumor cells, a cell survival role for sortilin can be deduced from these results. In conclusion, the potency of apoptosis induction via silencing of sortilin expression in tumor cells may introduce sortilin as a potential candidate for developing a novel targeted therapy in patients with ovarian carcinoma.
Language	English
Publishing date	2014-08-17
Publishing country	Iran
Document type	Journal Article
ZDB-ID	2520683-7
ISSN	2008-4625 ; 2008-2835
ISSN (online)	2008-4625
ISSN	2008-2835
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: Ectopic Expression of Sortilin 1 (NTR-3) in Patients with Ovarian Carcinoma.

Hemmati, Shayda / Zarnani, Amir Hassan / Mahmoudi, Ahmad Reza / Sadeghi, Mohammad-Reza / Soltanghoraee, Haleh / Akhondi, Mohammad Mehdi / Tarahomi, Majid / Jeddi-Tehrani, Mahmood / Rabbani, Hodjattallah

Avicenna journal of medical biotechnology

2013 Volume 1, Issue 2, Page(s) 125–131

Abstract: Gene expression profiling of ovarian carcinoma tissues has shown an increase of four-fold expression of SORT1 gene. Sortilin 1 (NTR-3) is a 95-100 kDa protein normally expressed in heart, brain, placenta, skeletal muscle, spinal cord, thyroid, and testis. ...

Abstract	Gene expression profiling of ovarian carcinoma tissues has shown an increase of four-fold expression of SORT1 gene. Sortilin 1 (NTR-3) is a 95-100 kDa protein normally expressed in heart, brain, placenta, skeletal muscle, spinal cord, thyroid, and testis. However, its expression has never been reported in normal ovary. Here, we report expression of sortilin 1 in ovarian carcinoma tissues both at gene and protein levels. Sortilin 1 was expressed in all ovarian carcinoma patients (n=15) as well as ovarian carcinoma cell lines (n=5) regardless of their phenotypic characteristics. Non-malignant ovaries (n=6) did not express sortilin 1. The molecular basis for this ectopic expression is not yet clear. Our results showed a major cell surface expression of sortilin 1 rather than ER-Golgi compartment where it is mainly expressed. This finding may introduce sortilin 1 as a novel tumor marker for diagnosis of ovarian carcinoma and may signify its therapeutic value in targeted therapy.
Language	English
Publishing date	2013-02-12
Publishing country	Iran
Document type	Journal Article
ZDB-ID	2520683-7
ISSN	2008-4625 ; 2008-2835
ISSN (online)	2008-4625
ISSN	2008-2835
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: EVI1 inhibits apoptosis induced by antileukemic drugs via upregulation of CDKN1A/p21/WAF in human myeloid cells.

Rommer, Anna / Steinmetz, Birgit / Herbst, Friederike / Hackl, Hubert / Heffeter, Petra / Heilos, Daniela / Filipits, Martin / Steinleitner, Katarina / Hemmati, Shayda / Herbacek, Irene / Schwarzinger, Ilse / Hartl, Katharina / Rondou, Pieter / Glimm, Hanno / Karakaya, Kadin / Krämer, Alwin / Berger, Walter / Wieser, Rotraud

PloS one

2013 Volume 8, Issue 2, Page(s) e56308

Abstract: Overexpression of ecotropic viral integration site 1 (EVI1) is associated with aggressive disease in acute myeloid leukemia (AML). Despite of its clinical importance, little is known about the mechanism through which EVI1 confers resistance to ... ...

Abstract	Overexpression of ecotropic viral integration site 1 (EVI1) is associated with aggressive disease in acute myeloid leukemia (AML). Despite of its clinical importance, little is known about the mechanism through which EVI1 confers resistance to antileukemic drugs. Here, we show that a human myeloid cell line constitutively overexpressing EVI1 after infection with a retroviral vector (U937_EVI1) was partially resistant to etoposide and daunorubicin as compared to empty vector infected control cells (U937_vec). Similarly, inducible expression of EVI1 in HL-60 cells decreased their sensitivity to daunorubicin. Gene expression microarray analyses of U937_EVI1 and U937_vec cells cultured in the absence or presence of etoposide showed that 77 and 419 genes were regulated by EVI1 and etoposide, respectively. Notably, mRNA levels of 26 of these genes were altered by both stimuli, indicating that EVI1 regulated genes were strongly enriched among etoposide regulated genes and vice versa. One of the genes that were induced by both EVI1 and etoposide was CDKN1A/p21/WAF, which in addition to its function as a cell cycle regulator plays an important role in conferring chemotherapy resistance in various tumor types. Indeed, overexpression of CDKN1A in U937 cells mimicked the phenotype of EVI1 overexpression, similarly conferring partial resistance to antileukemic drugs.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Apoptosis/drug effects ; Cell Differentiation/drug effects ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Daunorubicin/pharmacology ; Drug Resistance, Neoplasm ; Etoposide/pharmacology ; Female ; Humans ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Myeloid, Acute/metabolism ; Leukemia, Myeloid, Acute/pathology ; MDS1 and EVI1 Complex Locus Protein ; Mice ; Myeloid Cells/drug effects ; Myeloid Cells/metabolism ; Myeloid Cells/pathology ; Proto-Oncogenes/genetics ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Up-Regulation/drug effects
Chemical Substances	Antineoplastic Agents ; Cyclin-Dependent Kinase Inhibitor p21 ; DNA-Binding Proteins ; MDS1 and EVI1 Complex Locus Protein ; MECOM protein, human ; Transcription Factors ; Etoposide (6PLQ3CP4P3) ; Daunorubicin (ZS7284E0ZP)
Language	English
Publishing date	2013-02-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0056308
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.

To top

More links

Kategorien

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

Inter-library loan at ZB MED

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED