Breakpoint cluster region-c-abl oncogene 1, non-receptor tyrosine kinase signaling: Current patterns of the versatile regulator revisited

Rana, Aamir; Ali, Ghulam Muhammad; Ali, Shaukat; Khan, Ammara; Sabiha, Bibi; Malik, Shazia; Riaz, Afshan; Farooqı, Ammad Ahmad

doi:10.4103/0973-1482.110338

Cited by 4 publications

(2 citation statements)

References 24 publications

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“…These results clearly indicate that BV02 could represent a valid option for the treatment of CML, particularly of Imatinib-resistant forms [107]. Since then, BV02 has been used as reference inhibitor of 14-3-3 PPIs in many researches [117][118][119][120]. However, a hydration/dehydration pathway that generates the corresponding phthalimide derivative 9 and vice versa (Figure 5) was recently identified as the possible mechanism of BV02 chemical instability.…”

Section: Non-covalent Small Molecule Inhibitors Of 14-3-3 Ppismentioning

confidence: 98%

Structure, Function, Involvement in Diseases and Targeting of 14-3-3 Proteins: An Update

Cau

Valensin

Mori

et al. 2018

CMC

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14-3-3 is a class of proteins able to interact with a multitude of targets by establishing protein-protein interactions (PPIs). They are usually found in all eukaryotes with a conserved secondary structure and high sequence homology among species. 14-3-3 proteins are involved in many physiological and pathological cellular processes either by triggering or interfering with the activity of specific protein partners. In the last years, the scientific community has collected many evidences on the role played by seven human 14-3-3 isoforms in cancer or neurodegenerative diseases. Indeed, these proteins regulate the molecular mechanisms associated to these diseases by interacting with (i) oncogenic and (ii) pro-apoptotic proteins and (iii) with proteins involved in Parkinson and Alzheimer diseases. The discovery of small molecule modulators of 14-3-3 PPIs could facilitate complete understanding of the physiological role of these proteins, and might offer valuable therapeutic approaches for these critical pathological states.

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Section: Non-covalent Small Molecule Inhibitors Of 14-3-3 Ppismentioning

confidence: 98%

Structure, Function, Involvement in Diseases and Targeting of 14-3-3 Proteins: An Update

Cau

Valensin

Mori

et al. 2018

CMC

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“…This chromosome is a result of a reciprocal translocation between the long arms of chromosomes 9 and 22 t(9;22)(q34;q11), leading to BCR-ABL1 fusion gene with constitutive tyrosine kinase activity (Nowell & Hungerford, 1960). The breakpoint within the ABL1 gene (GenBank accession NC_000009.12) is almost always at the second exon (a2), while the breakpoint in the BCR gene varies and can be localized to one of the three regions: major breakpoint cluster region (M-BCR), minor BCR (m-BCR), and micro-BCR (Burmeister & Reinhardt, 2008;Rana et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Association of BCR/ABL transcript variants with different blood parameters and demographic features in Iraqi chronic myeloid leukemia patients

Khazaal

Hamdan

Al-Mayah

2019

Molec Gen & Gen Med

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Background Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm characterized by the presence of BCR‐ABL fusion gene (GenBank accession ). In the vast majority of CML patients, the typical subtype of BCR‐ABL transcript are b3a2, b2a2 or both. The aim of this study was to determine the different subtypes of BCR‐ABL transcript and their impact on the demographic and hematological parameters in Iraqi patients with CML. Methods One hundred patients with chronic phase CML (11 newly diagnosed and 89 imatinib‐resistant) were enrolled in this study. Ribonucleic acid (RNA) was extracted from leukocytes, and complementary DNA was created using reverse transcriptase polymerase chain reaction technique. A multiplex polymerase chain reaction with four specific primers was used to determine the BCR‐ABL fusion subtypes in each patient. Results Male to female ratio was 1.38:1. Fifty‐nine patients expressed b3a2 transcript, whereas 39 of the remaining cases were positive for b2a2 variant. One case expressed b2a3 transcript, while the last case coexpressed the two subtypes of mRNA b3a2/b2a2. Male and female were significantly associated with b3a2 and b2a2 subtypes, respectively. The b3a2 subtype showed higher total leukocyte count than b2a2 subgroup, while b2a2 variant demonstrated significantly elevated platelet counts compared to those with b3a2 transcript. A significantly higher plateletcrit percentage (PCT%) was found in patients with b2a2 transcript whereas. Conclusions The testified Iraqi group expressed M‐BCR‐ABL type with preponderance of b3a2 over b2a2 subtype. There was a gender‐skewed distribution in BCR‐ABL transcript types with b3a2 transcript more prevalent in males. The type of BCR‐ABL transcript is reflected by different leukocyte and platelet counts at diagnosis, which might represent a distinct phenotype and disease biology.

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Molecular insights to the bioactive form of BV02 , a reference inhibitor of 14-3-3σ protein–protein interactions

Valensin

Cau

Calandro

et al. 2016

Bioorganic & Medicinal Chemistry Letters

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Breakpoint cluster region-c-abl oncogene 1, non-receptor tyrosine kinase signaling: Current patterns of the versatile regulator revisited

Cited by 4 publications

References 24 publications

Structure, Function, Involvement in Diseases and Targeting of 14-3-3 Proteins: An Update

Structure, Function, Involvement in Diseases and Targeting of 14-3-3 Proteins: An Update

Association of BCR/ABL transcript variants with different blood parameters and demographic features in Iraqi chronic myeloid leukemia patients

Molecular insights to the bioactive form of BV02 , a reference inhibitor of 14-3-3σ protein–protein interactions

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