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Mouse Anti-FIP1L1 Recombinant Antibody (CBXF-3033) (CBMAB-F3739-CQ)

This product is a mouse antibody that recognizes FIP1L1. The antibody CBXF-3033 can be used for immunoassay techniques such as: ELISA, WB.
See all FIP1L1 antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
CBXF-3033
Antibody Isotype
IgG1, κ
Application
ELISA, WB

Basic Information

Immunogen
Full length recombinant corresponding to aa1-379 from human FIP1L1 (AAH17724) with GST tag
Specificity
Human
Antibody Isotype
IgG1, κ
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Buffer
PBS, pH 7.2
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
FIP1 like 1 (S. cerevisiae)
Introduction
This gene encodes a subunit of the CPSF (cleavage and polyadenylation specificity factor) complex that polyadenylates the 3' end of mRNA precursors. This gene, the homolog of yeast Fip1 (factor interacting with PAP), binds to U-rich sequences of pre-mRNA and stimulates poly(A) polymerase activity. Its N-terminus contains a PAP-binding site and its C-terminus an RNA-binding domain. An interstitial chromosomal deletion on 4q12 creates an in-frame fusion of human genes FIP1L1 and PDGFRA (platelet-derived growth factor receptor, alpha). The FIP1L1-PDGFRA fusion gene encodes a constitutively activated tyrosine kinase that joins the first 233 amino acids of FIP1L1 to the last 523 amino acids of PDGFRA. This gene fusion and chromosomal deletion is the cause of some forms of idiopathic hypereosinophilic syndrome (HES). This syndrome, recently reclassified as chronic eosinophilic leukemia (CEL), is responsive to treatment with tyrosine kinase inhibitors. Alternative splicing results in multiple transcript variants encoding distinct isoforms.
Entrez Gene ID
81608
UniProt ID
Q6UN15
Alternative Names
Factor Interacting With PAPOLA And CPSF1; FIP1L1 Cleavage And Polyadenylation Specific Factor Subunit; Rearranged In Hypereosinophilia; Factor Interacting With PAP; FIP1-Like 1 Protein; HFip1; FIP1;
Function
Component of the cleavage and polyadenylation specificity factor (CPSF) complex that plays a key role in pre-mRNA 3'-end formation, recognizing the AAUAAA signal sequence and interacting with poly(A) polymerase and other factors to bring about cleavage and poly(A) addition. FIP1L1 contributes to poly(A) site recognition and stimulates poly(A) addition. Binds to U-rich RNA sequence elements surrounding the poly(A) site. May act to tether poly(A) polymerase to the CPSF complex.
Biological Process
mRNA polyadenylation Source: GO_Central
Pre-mRNA cleavage required for polyadenylation Source: GO_Central
Cellular Location
Nucleus
Involvement in disease
A chromosomal aberration involving FIP1L1 is found in some cases of hypereosinophilic syndrome. Interstitial chromosomal deletion del(4)(q12q12) causes the fusion of FIP1L1 and PDGFRA (FIP1L1-PDGFRA).

Miltiadous, O., Petrova-Drus, K., Kaicker, S., Mathew, S., Kluk, M., Geyer, J. T., ... & Shukla, N. (2022). Successful treatment and integrated genomic analysis of an infant with FIP1L1-RARA fusion–associated myeloid neoplasm. Blood advances, 6(4), 1137-1142.

Wang, Y., Rui, Y., Shen, Y., Li, J., Liu, P., Lu, Q., & Fang, Y. (2021). Myeloid sarcoma type of acute promyelocytic leukemia with a cryptic insertion of RARA into FIP1L1: the clinical utility of NGS and bioinformatic analyses. Frontiers in Oncology, 11, 688203.

Tennenbaum, J., Groh, M., Venditti, L., Campos-Gazeau, F., Chalayer, E., De Broucker, T., ... & Rohmer, J. (2021). FIP1L1-PDGFRA-associated hypereosinophilic syndrome as a treatable cause of watershed infarction.

Dong, W., Liu, X., Yang, C., Wang, D., Xue, Y., Ruan, X., ... & Liu, Y. (2021). Glioma glycolipid metabolism: MSI2–SNORD12B–FIP1L1–ZBTB4 feedback loop as a potential treatment target. Clinical and Translational Medicine, 11(5), e411.

Rohmer, J., Couteau‐Chardon, A., Trichereau, J., Panel, K., Gesquiere, C., Ben Abdelali, R., ... & Zini, J. M. (2020). Epidemiology, clinical picture and long‐term outcomes of FIP1L1‐PDGFRA‐positive myeloid neoplasm with eosinophilia: Data from 151 patients. American Journal of Hematology, 95(11), 1314-1323.

Metzgeroth, G., Schwaab, J., Naumann, N., Jawhar, M., Haferlach, T., Fabarius, A., ... & Reiter, A. (2020). Treatment-free remission in FIP1L1-PDGFRA–positive myeloid/lymphoid neoplasms with eosinophilia after imatinib discontinuation. Blood Advances, 4(3), 440-443.

Yang, Y., Lin, H., Du, Z., Hu, R., Tang, Y., Liang, X., ... & Tan, Y. (2020). Imatinib therapy in acute myeloid leukemia with DEK‑NUP214 and FIP1L1‑PDGFRA rearrangement: A case report. Oncology Letters, 19(5), 3587-3592.

Helbig, G., Lewandowski, K., Świderska, A., Rodzaj, M., Seferyńska, I., & Gajkowska-Kulik, J. (2020). Exquisite response to imatinib mesylate in FIP1L1-PDGFRA-mutated hypereosinophilic syndrome: a 12-year experience of the Polish Hypereosinophilic Syndrome Study Group. Pol Arch Intern Med, 130(3), 255-257.

Srinivasan, A., Scordino, T., & Baker, A. (2019). Myeloid neoplasm with eosinophilia and FIP1L1-PDGFRA rearrangement treated with imatinib mesylate: a pediatric case with long-term follow-up. Journal of Pediatric Hematology/Oncology, 41(4), 334-335.

Berto, D., Santos, A., Camiña, R. H., Machado, E. S., & Baptistella, A. R. (2018). FIP1L1‑PDGFRA fusion‑negative hypereosinophilic syndrome with uncommon cardiac involvement responding to imatinib treatment: A case report. Molecular and Clinical Oncology, 9(1), 35-39.

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For research use only. Not intended for any clinical use.

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