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Article ; Online: p53 Family in Resistance to Targeted Therapy of Melanoma

Ignacija Vlašić / Anđela Horvat / Ana Tadijan / Neda Slade

International Journal of Molecular Sciences, Vol 24, Iss 1, p

2022 Volume 65

Abstract: Metastatic melanoma is one of the most aggressive tumors, with frequent mutations affecting components of the MAPK pathway, mainly protein kinase BRAF. Despite promising initial response to BRAF inhibitors, melanoma progresses due to development of ... ...

Abstract	Metastatic melanoma is one of the most aggressive tumors, with frequent mutations affecting components of the MAPK pathway, mainly protein kinase BRAF. Despite promising initial response to BRAF inhibitors, melanoma progresses due to development of resistance. In addition to frequent reactivation of MAPK or activation of PI3K/AKT signaling pathways, recently, the p53 pathway has been shown to contribute to acquired resistance to targeted MAPK inhibitor therapy. Canonical tumor suppressor p53 is inactivated in melanoma by diverse mechanisms. The TP53 gene and two other family members, TP63 and TP73 , encode numerous protein isoforms that exhibit diverse functions during tumorigenesis. The p53 family isoforms can be produced by usage of alternative promoters and/or splicing on the C- and N-terminus. Various p53 family isoforms are expressed in melanoma cell lines and tumor samples, and several of them have already shown to have specific functions in melanoma, affecting proliferation, survival, metastatic potential, invasion, migration, and response to therapy. Of special interest are p53 family isoforms with increased expression and direct involvement in acquired resistance to MAPK inhibitors in melanoma cells, implying that modulating their expression or targeting their functional pathways could be a potential therapeutic strategy to overcome resistance to MAPK inhibitors in melanoma.
Keywords	melanoma ; MAPK inhibitors ; resistance ; p53 ; p63 ; p73 ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	572
Language	English
Publishing date	2022-12-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: p53/p73 Protein Network in Colorectal Cancer and Other Human Malignancies.

Horvat, Anđela / Tadijan, Ana / Vlašić, Ignacija / Slade, Neda

Cancers

2021 Volume 13, Issue 12

Abstract: The p53 tumor suppressor protein is crucial for cell growth control and the maintenance of genomic stability. Later discovered, p63 and p73 share structural and functional similarity with p53. To understand the p53 pathways more profoundly, all family ... ...

Abstract	The p53 tumor suppressor protein is crucial for cell growth control and the maintenance of genomic stability. Later discovered, p63 and p73 share structural and functional similarity with p53. To understand the p53 pathways more profoundly, all family members should be considered. Each family member possesses two promoters and alternative translation initiation sites, and they undergo alternative splicing, generating multiple isoforms. The resulting isoforms have important roles in carcinogenesis, while their expression is dysregulated in several human tumors including colorectal carcinoma, which makes them potential targets in cancer treatment. Their activities arise, at least in part, from the ability to form tetramers that bind to specific DNA sequences and activate the transcription of target genes. In this review, we summarize the current understanding of the biological activities and regulation of the p53/p73 isoforms, highlighting their role in colorectal tumorigenesis. The analysis of the expression patterns of the p53/p73 isoforms in human cancers provides an important step in the improvement of cancer therapy. Furthermore, the interactions among the p53 family members which could modulate normal functions of the canonical p53 in tumor tissue are described. Lastly, we emphasize the importance of clinical studies to assess the significance of combining the deregulation of different members of the p53 family to define the outcome of the disease.
Language	English
Publishing date	2021-06-09
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13122885
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Article ; Online: Characterization of Vemurafenib-Resistant Melanoma Cell Lines Reveals Novel Hallmarks of Targeted Therapy Resistance.

Radić, Martina / Vlašić, Ignacija / Jazvinšćak Jembrek, Maja / Horvat, Anđela / Tadijan, Ana / Sabol, Maja / Dužević, Marko / Herak Bosnar, Maja / Slade, Neda

International journal of molecular sciences

2022 Volume 23, Issue 17

Abstract: Regardless of the significant improvements in treatment of melanoma, the majority of patients develop resistance whose mechanisms are still not completely understood. Hence, we generated and characterized two melanoma-derived cell lines, primary WM793B ... ...

Abstract	Regardless of the significant improvements in treatment of melanoma, the majority of patients develop resistance whose mechanisms are still not completely understood. Hence, we generated and characterized two melanoma-derived cell lines, primary WM793B and metastatic A375M, with acquired resistance to the RAF inhibitor vemurafenib. The morphology of the resistant primary WM793B melanoma cells showed EMT-like features and exhibited a hybrid phenotype with both epithelial and mesenchymal characteristics. Surprisingly, the vemurafenib-resistant melanoma cells showed a decreased migration ability but also displayed a tendency to collective migration. Signaling pathway analysis revealed the reactivation of MAPK and the activation of the PI3K/AKT pathway depending on the vemurafenib-resistant cell line. The acquired resistance to vemurafenib caused resistance to chemotherapy in primary WM793B melanoma cells. Furthermore, the cell-cycle analysis and altered levels of cell-cycle regulators revealed that resistant cells likely transiently enter into cell cycle arrest at the G0/G1 phase and gain slow-cycling cell features. A decreased level of NME1 and NME2 metastasis suppressor proteins were found in WM793B-resistant primary melanoma, which is possibly the result of vemurafenib-acquired resistance and is one of the causes of increased PI3K/AKT signaling. Further studies are needed to reveal the vemurafenib-dependent negative regulators of NME proteins, their role in PI3K/AKT signaling, and their influence on vemurafenib-resistant melanoma cell characteristics.
MeSH term(s)	Cell Line, Tumor ; Drug Resistance, Neoplasm/genetics ; Humans ; Indoles/pharmacology ; Indoles/therapeutic use ; Melanoma/drug therapy ; Melanoma/genetics ; Melanoma/pathology ; Phosphatidylinositol 3-Kinases ; Proto-Oncogene Proteins B-raf/genetics ; Proto-Oncogene Proteins B-raf/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Sulfonamides/pharmacology ; Sulfonamides/therapeutic use ; Vemurafenib/pharmacology ; Vemurafenib/therapeutic use
Chemical Substances	Indoles ; Sulfonamides ; Vemurafenib (207SMY3FQT) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2022-08-31
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23179910
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Article ; Online: Characterization of Vemurafenib-Resistant Melanoma Cell Lines Reveals Novel Hallmarks of Targeted Therapy Resistance

Martina Radić / Ignacija Vlašić / Maja Jazvinšćak Jembrek / Anđela Horvat / Ana Tadijan / Maja Sabol / Marko Dužević / Maja Herak Bosnar / Neda Slade

International Journal of Molecular Sciences, Vol 23, Iss 9910, p

2022 Volume 9910

Abstract	Regardless of the significant improvements in treatment of melanoma, the majority of patients develop resistance whose mechanisms are still not completely understood. Hence, we generated and characterized two melanoma-derived cell lines, primary WM793B and metastatic A375M, with acquired resistance to the RAF inhibitor vemurafenib. The morphology of the resistant primary WM793B melanoma cells showed EMT-like features and exhibited a hybrid phenotype with both epithelial and mesenchymal characteristics. Surprisingly, the vemurafenib-resistant melanoma cells showed a decreased migration ability but also displayed a tendency to collective migration. Signaling pathway analysis revealed the reactivation of MAPK and the activation of the PI3K/AKT pathway depending on the vemurafenib-resistant cell line. The acquired resistance to vemurafenib caused resistance to chemotherapy in primary WM793B melanoma cells. Furthermore, the cell-cycle analysis and altered levels of cell-cycle regulators revealed that resistant cells likely transiently enter into cell cycle arrest at the G0/G1 phase and gain slow-cycling cell features. A decreased level of NME1 and NME2 metastasis suppressor proteins were found in WM793B-resistant primary melanoma, which is possibly the result of vemurafenib-acquired resistance and is one of the causes of increased PI3K/AKT signaling. Further studies are needed to reveal the vemurafenib-dependent negative regulators of NME proteins, their role in PI3K/AKT signaling, and their influence on vemurafenib-resistant melanoma cell characteristics.
Keywords	melanoma ; vemurafenib ; drug resistance ; signaling pathways ; epithelial–mesenchymal transition (EMT) ; slow-cycling cells ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	570
Language	English
Publishing date	2022-08-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: The Subcellular Localization and Oligomerization Preferences of NME1/NME2 upon Radiation-Induced DNA Damage.

Radić, Martina / Šoštar, Marko / Weber, Igor / Ćetković, Helena / Slade, Neda / Herak Bosnar, Maja

International journal of molecular sciences

2020 Volume 21, Issue 7

Abstract: Nucleoside diphosphate kinases (NDPK/NME/Nm23) are enzymes composed of subunits NME1/NDPK A and NME2/NDPK B, responsible for the maintenance of the cellular (d)NTP pool and involved in other cellular processes, such as metastasis suppression and DNA ... ...

Abstract	Nucleoside diphosphate kinases (NDPK/NME/Nm23) are enzymes composed of subunits NME1/NDPK A and NME2/NDPK B, responsible for the maintenance of the cellular (d)NTP pool and involved in other cellular processes, such as metastasis suppression and DNA damage repair. Although eukaryotic NDPKs are active only as hexamers, it is unclear whether other NME functions require the hexameric form, and how the isoenzyme composition varies in different cellular compartments. To examine the effect of DNA damage on intracellular localization of NME1 and NME2 and the composition of NME oligomers in the nucleus and the cytoplasm, we used live-cell imaging and the FRET/FLIM technique. We showed that exogenous NME1 and NME2 proteins co-localize in the cytoplasm of non-irradiated cells, and move simultaneously to the nucleus after gamma irradiation. The FRET/FLIM experiments imply that, after DNA damage, there is a slight shift in the homomer/heteromer balance between the nucleus and the cytoplasm. Collectively, our results indicate that, after irradiation, NME1 and NME2 engage in mutual functions in the nucleus, possibly performing specific functions in their homomeric states. Finally, we demonstrated that fluorophores fused to the N-termini of NME polypeptides produce the largest FRET effect and thus recommend this orientation for use in similar studies.
MeSH term(s)	Animals ; Biomarkers ; Cell Line ; Cell Nucleus/metabolism ; DNA Damage/genetics ; DNA Damage/radiation effects ; Fluorescent Antibody Technique ; Gamma Rays ; Humans ; NM23 Nucleoside Diphosphate Kinases/chemistry ; NM23 Nucleoside Diphosphate Kinases/genetics ; NM23 Nucleoside Diphosphate Kinases/metabolism ; Protein Binding ; Protein Multimerization ; Protein Transport ; Radiation, Ionizing
Chemical Substances	Biomarkers ; NM23 Nucleoside Diphosphate Kinases ; NME1 protein, human (EC 2.7.4.6) ; NME2 protein, human (EC 2.7.4.6)
Language	English
Publishing date	2020-03-29
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21072363
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Article ; Online: The Subcellular Localization and Oligomerization Preferences of NME1/NME2 upon Radiation-Induced DNA Damage

Martina Radić / Marko Šoštar / Igor Weber / Helena Ćetković / Neda Slade / Maja Herak Bosnar

International Journal of Molecular Sciences, Vol 21, Iss 7, p

2020 Volume 2363

Abstract	Nucleoside diphosphate kinases (NDPK/NME/Nm23) are enzymes composed of subunits NME1/NDPK A and NME2/NDPK B, responsible for the maintenance of the cellular (d)NTP pool and involved in other cellular processes, such as metastasis suppression and DNA damage repair. Although eukaryotic NDPKs are active only as hexamers, it is unclear whether other NME functions require the hexameric form, and how the isoenzyme composition varies in different cellular compartments. To examine the effect of DNA damage on intracellular localization of NME1 and NME2 and the composition of NME oligomers in the nucleus and the cytoplasm, we used live-cell imaging and the FRET/FLIM technique. We showed that exogenous NME1 and NME2 proteins co-localize in the cytoplasm of non-irradiated cells, and move simultaneously to the nucleus after gamma irradiation. The FRET/FLIM experiments imply that, after DNA damage, there is a slight shift in the homomer/heteromer balance between the nucleus and the cytoplasm. Collectively, our results indicate that, after irradiation, NME1 and NME2 engage in mutual functions in the nucleus, possibly performing specific functions in their homomeric states. Finally, we demonstrated that fluorophores fused to the N-termini of NME polypeptides produce the largest FRET effect and thus recommend this orientation for use in similar studies.
Keywords	NME ; NDPK ; Nm23 ; nucleoside diphosphate kinase ; FRET ; FLIM ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	571
Language	English
Publishing date	2020-03-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The interactions of p53 with tau and Aß as potential therapeutic targets for Alzheimer's disease.

Jazvinšćak Jembrek, Maja / Slade, Neda / Hof, Patrick R / Šimić, Goran

Progress in neurobiology

2018 Volume 168, Page(s) 104–127

Abstract: Alzheimer's disease (AD), the most common progressive neurodegenerative disorder, is characterized by severe cognitive decline and personality changes as a result of synaptic and neuronal loss. The defining clinicopathological hallmarks of the disease ... ...

Abstract	Alzheimer's disease (AD), the most common progressive neurodegenerative disorder, is characterized by severe cognitive decline and personality changes as a result of synaptic and neuronal loss. The defining clinicopathological hallmarks of the disease are deposits of amyloid precursor protein (APP)-derived amyloid-β peptides (Aβ) in the brain parenchyma, and intracellular aggregates of truncated and hyperphosphorylated tau protein in neurofibrillary tangles (NFT). At the cellular and molecular levels, many intertwined pathological mechanisms that relate Aβ and tau pathology with a transcription factor p53 have been revealed. p53 is activated in response to various stressors that threaten genomic stability. Depending on damage severity, it promotes neuronal death or survival, predominantly via transcription-dependent mechanisms that affect expression of apoptosis-related target genes. Levels of p53 are enhanced in the AD brain and maintain sustained tau hyperphosphorylation, whereas intracellular Aβ directly contributes to p53 pool and promotes downstream p53 effects. The review summarizes the role of p53 in neuronal function, discusses the interactions of p53, tau, and Aβ in the normal brain and during the progression of AD pathology, and considers the impact of the most prominent hereditary risk factors of AD on p53/tau/Aβ interactions. A better understanding of this intricate interplay would provide deeper insight into AD pathology and might offer some novel therapeutic targets for the improvement of treatment options. In this regard, drugs and natural compounds targeting the p53 pathway are of growing interest in neuroprotection as they may represent promising therapeutic approaches in the prevention of oxidative stress-dependent pathological processes underlying AD.
MeSH term(s)	Alzheimer Disease/metabolism ; Alzheimer Disease/therapy ; Amyloid beta-Peptides/metabolism ; Animals ; Humans ; Tumor Suppressor Protein p53/metabolism ; tau Proteins/metabolism
Chemical Substances	Amyloid beta-Peptides ; Tumor Suppressor Protein p53 ; tau Proteins
Language	English
Publishing date	2018-05-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	185535-9
ISSN	1873-5118 ; 0301-0082
ISSN (online)	1873-5118
ISSN	0301-0082
DOI	10.1016/j.pneurobio.2018.05.001
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Article: Altered Expression of Shorter p53 Family Isoforms Can Impact Melanoma Aggressiveness.

Tadijan, Ana / Precazzini, Francesca / Hanžić, Nikolina / Radić, Martina / Gavioli, Nicolò / Vlašić, Ignacija / Ozretić, Petar / Pinto, Lia / Škreblin, Lidija / Barban, Giulia / Slade, Neda / Ciribilli, Yari

Cancers

2021 Volume 13, Issue 20

Abstract: Cutaneous melanoma is the most aggressive form of skin cancer. Despite the significant advances in the management of melanoma in recent decades, it still represents a challenge for clinicians. ... ...

Abstract	Cutaneous melanoma is the most aggressive form of skin cancer. Despite the significant advances in the management of melanoma in recent decades, it still represents a challenge for clinicians. The
Language	English
Publishing date	2021-10-18
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13205231
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Article ; Online: Targeting p73--a potential approach in cancer treatment.

Slade, Neda / Horvat, Anđela

Current pharmaceutical design

2011 Volume 17, Issue 6, Page(s) 591–602

Abstract: The p53 family consists of three members: p53, p63 and p73. All three of them have a role in cell cycle arrest and induction of apoptosis. However, despite structural and partly functional similarity, there are striking differences in their functions and ...

Abstract	The p53 family consists of three members: p53, p63 and p73. All three of them have a role in cell cycle arrest and induction of apoptosis. However, despite structural and partly functional similarity, there are striking differences in their functions and each of them has its own and unique identity. All three genes encode multiple variants with opposing functions in cancer development - full length transactivation forms with proapoptotic and antiproliferative functions, and dominant-negative transactivation-deficient forms with anti-apoptotic (oncogenic) functions. The functional interactions between family members are crucial to gain insight and understand their role in cancer biology. The discovery of p53/p73 network could have a major clinical impact in prognostic use and targeted drug design. In the current review we present the recent achievements in p73 research including very complex and sophisticated p73 regulation and response to DNA damage, and functional interactions among family members. We discuss how p73 has affected drug discovery. According to the p73 tumor suppressor function, we outline current aspects of anticancer therapy.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; DNA-Binding Proteins/antagonists & inhibitors ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Drug Resistance, Neoplasm ; Humans ; Molecular Targeted Therapy ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism ; Nuclear Proteins/antagonists & inhibitors ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Tumor Protein p73 ; Tumor Suppressor Protein p53/metabolism ; Tumor Suppressor Proteins/antagonists & inhibitors ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism
Chemical Substances	Antineoplastic Agents ; DNA-Binding Proteins ; Nuclear Proteins ; TP73 protein, human ; Tumor Protein p73 ; Tumor Suppressor Protein p53 ; Tumor Suppressor Proteins
Language	English
Publishing date	2011-03-08
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1304236-1
ISSN	1873-4286 ; 1381-6128
ISSN (online)	1873-4286
ISSN	1381-6128
DOI	10.2174/138161211795222621
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Zs.A 4714: Show issues

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Article ; Online: The role of p53 isoforms' expression and p53 mutation status in renal cell cancer prognosis.

Knezović Florijan, Marijana / Ozretić, Petar / Bujak, Maro / Pezzè, Laura / Ciribilli, Yari / Kaštelan, Željko / Slade, Neda / Hudolin, Tvrtko

Urologic oncology

2019 Volume 37, Issue 9, Page(s) 578.e1–578.e10

Abstract: Objectives: To analyze p53 mutations and gene expression of p53, ∆40p53, and ∆133p53 isoforms in renal cell cancer (RCC) tissues and normal adjacent tissue (NAT) and to associate them to clinical features and outcome.: Patients and methods: Forty-one ...

Abstract	Objectives: To analyze p53 mutations and gene expression of p53, ∆40p53, and ∆133p53 isoforms in renal cell cancer (RCC) tissues and normal adjacent tissue (NAT) and to associate them to clinical features and outcome. Patients and methods: Forty-one randomly selected patients, with primary, previously untreated RCC, with complete clinicopathohistological data were analyzed. NAT samples were available for 37 cases. Expression of p53, ∆40p53 and ∆133p53 was determined using RT-qPCR. A functional yeast-based assay was performed to analyze p53 mutations. Results: More than half (56.1%) of patients harbored functional p53 mutations, and they were significantly younger than those with wild type (WT) p53 (P = 0.032). Expression of p53, ∆40p53, and ∆133p53 was upregulated in mutant (MT) p53 RCC compared to WT p53 RCC tissues. However, there was no difference in expression of these isoforms between MT p53 RCC tissues and NAT. Expression of ∆133p53 was significantly downregulated in WT p53 tissues compared to NAT (P = 0.006). Patients that harbored functional p53 mutation had better overall survival (hazard ratio 4.32, 95% confidence interval 1.46-18.82, P = 0.006). Multivariate analysis demonstrated that tumor stage and p53 mutation might be used as independent prognostic marker for overall survival in RCC patients. Conclusions: Our findings support the specific events in the carcinogenesis of RCC. p53 isoforms can be differentially expressed depending on p53 mutational status.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Carcinoma, Renal Cell/genetics ; Carcinoma, Renal Cell/metabolism ; Carcinoma, Renal Cell/pathology ; Female ; Humans ; Kidney Neoplasms/genetics ; Kidney Neoplasms/metabolism ; Male ; Middle Aged ; Mutation ; Prognosis ; Prospective Studies ; Protein Isoforms ; Tumor Suppressor Protein p53/biosynthesis ; Tumor Suppressor Protein p53/genetics
Chemical Substances	Protein Isoforms ; TP53 protein, human ; Tumor Suppressor Protein p53
Language	English
Publishing date	2019-04-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1336505-8
ISSN	1873-2496 ; 1078-1439
ISSN (online)	1873-2496
ISSN	1078-1439
DOI	10.1016/j.urolonc.2019.03.007
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