ABL1 (Phospho-Thr735) ELISA Kit (DEIA-XYA152)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
2 x 96T
Sample
cultured cells
Species Reactivity
Human, Mouse, Rat
Intended Use
The ABL1 (Phospho-Thr735) Cell-Based ELISA Kit is a convenient, lysate-free, high throughput and sensitive assay kit that can monitor ABL1 protein phosphorylation and expression profile in cells. The kit can be used for measuring the relative amounts of phosphorylated ABL1 in cultured cells as well as screening for the effects that various treatments, inhibitors (ie. siRNA or chemicals), or activators have on ABL1 phosphorylation.
Contents of Kit
1. 96-Well Cell Culture Clear-Bottom Microplate: 2 plates
2. 10x TBS: 24 mL (10x)
3. Quenching Buffer: 24 mL (1x)
4. Blocking Buffer: 50 mL (1x)
5. 10x Wash Buffer: 50 mL (10x)
6. 100x Anti-ABL1 (Phospho-Thr735) Antibody (Rabbit Polyclonal): 60 μL (100x), Red
7. 100x Anti-ABL1 Antibody (Rabbit Polyclonal): 60 μL (100x), Purple
8. 100x Anti-GAPDH Antibody (Mouse Monoclonal): 60 μL (100x), Green
9. HRP-Conjugated Anti-Rabbit IgG Antibody: 12 mL (1x), Glass
10. HRP-Conjugated Anti-Mouse IgG Antibody: 12 mL (1x), Glass
11. Primary Antibody Diluent: 12 mL (1x)
12. Ready-to-Use Substrate: 12 mL (1x), Brown
13. Stop Solution: 12 mL (1x)
14. Crystal Violet Solution: 12 mL (1x), Glass
15. SDS Solution: 24 mL (1x)
16. Adhesive Plate Seals: 4 seals
Storage
4°C/6 Months

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References


Breakpoint mapping of a t(9;22;12) chronic myeloid leukaemia patient with e14a3 BCR-ABL1 transcript using Nanopore sequencing

JOURNAL OF GENE MEDICINE

Authors: Zhao, Hu; Chen, Yuan; Shen, Chanjuan; Li, Lingshu; Li, Qingzhao; Tan, Kui; Huang, Huang; Hu, Guoyu

Background The genetic changes in chronic myeloid leukaemia (CML) have been well established, although challenges persist in cases with rare fusion transcripts or complex variant translocations. Here, we present a CML patient with e14a3 BCR-ABL1 transcript and t(9;22;12) variant Philadelphia (Ph) chromosome. Methods Cytogenetic analysis and fluorescencein situhybridization (FISH) was performed to identify the chromosomal aberrations and gene fusions. Rare fusion transcript was verified by a reverse transcription-polymerase chain reaction (RT-PCR). Breakpoints were characterized and validated using Oxford Nanopore Technologies (ONT) (Oxford, UK) and Sanger sequencing, respectively. Results The karyotype showed the translocation t(9;22;12)(q34;q11.2;q24) [20] and FISH indicated 40% positive BCR-ABL1 fusion signals. The RT-PCR suggested e14a3 type fusion transcript. The ONT sequencing analysis identified specific positions of translocation breakpoints: chr22:23633040-chr9:133729579, chr12:121567595-chr22:24701405, which were confirmed using Sanger sequencing. The patient achieved molecular remission 3 months after imatinib therapy. Conclusions The present study indicates Nanopore sequencing as a valid strategy, which can characterize breakpoints precisely in special clinical cases with atypical structural variations. CML patients with e14a3 transcripts may have good clinical course in the tyrosine kinase inhibitor era, as reviewed here.

A Rare Case of Systemic Mastocytosis with Associated Hematologic Neoplasm (SM-AHN) Involving Chronic Myeloid Leukemia: A Case Report and Literature Review

AMERICAN JOURNAL OF CASE REPORTS

Authors: Ibrahim, Feryal A.; Abdulla, Mohammad A. J.; Soliman, Dina; Al Sabbagh, Ahmad; Nawaz, Zafar; Akiki, Susanna Jane; Shwaylia, Hawraa; Yassin, Mohamed A.

Objective: Rare co-existance of disease or pathology Background: Single or multiple cell line dysplasia is a characteristic feature of myelodysplastic syndrome. However, significant dysgranulopoiesis is not a feature of chronic myeloid leukemia (CML). Systemic mastocytosis (SM) with an associated hematologic neoplasm (SM-AHN) comprises 5% to 40% of cases of SM. All types of hematologic neoplasms have been previously reported, although CML has been rarely encountered. Case Report: A 28-year-old male presented with a 3-month-history of weight loss and massive splenomegaly. Peripheral blood revealed marked leukocytosis, shift to left with 13% blasts. There was evident dysgranulopoiesis that raised a provisional diagnosis of myelodysplastic/myeloproliferative neoplasm. Bone marrow (BM) examination revealed granulocytic hyperplasia with 10% blasts and significant dysgranulopoiesis. Unexpectedly, cytogenetic analysis revealed t(9;22) with BCR/ABL1 rearrangement, diagnostic of chronic myeloid leukemia in an accelerated phase. The patient was started on dasatinib 100 mg upfront, however, he failed to respond, with increasing leukocytosis. Repeat BM examination showed persistence of the findings with 8% blasts. At this time, aggregates of mast cells with aberrant expression of CD25 were elicited, thus concluding the diagnosis of SM-AHN. The patient failed multiple lines of treatment (dasatinib, nilotinib, hydroxyurea, cytarabine subcutaneous, 6-mercaptopurine and interferon) and progressed to the blast phase a few months later. Conclusions: We report an unusual case of CML, presented with significant dysgranulopoiesis with an aggressive clinical course including SM uncovered during the disease course with subsequent transformation to the blast phase. The different biological behavior of this case underscores the need for studies on a larger number of cases to explore the significance of the aforementioned coexistent features.

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