Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Disruption of E627 and R683 interaction is responsible for B-cell acute lymphoblastic leukemia caused by JAK2 R683G(S) mutations.

Leukemia & lymphoma - 1 Dec 2013

Wu Qing-Yun, Guo Hua-Yan, Li Feng, Li Zhen-Yu, Zeng Ling-Yu, Xu Kai-Lin

Abstract excerpt

Janus kinase 2 (JAK2) is an important mediator of cytokine receptor signaling and plays key roles in hematopoietic and immune responses. The acquired JAK2 R683G(S) somatic mutations are detected in 15% of patients with B-cell acute lymphoblastic leukemia (B-ALL) and are presumed to be a biomarker for B-ALL. However, how JAK2 R683G(S) mutations lead to B-ALL is still unclear. Our results indicated that the E627...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cell Proliferation
Share to Codon
Share to Enzyme Activation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Erythropoietin

Share to Janus Kinase 2

Share to Precursor B-Cell Lymphoblastic Leukemia-Lymphoma

Share to Protein Conformation

Share to Protein Interaction Domains and Motifs

Source

Identifiers

PMID: 23452118
DOI: 10.3109/10428194.2013.781171

Genes

JAK2

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Disruption of E627 and R683 interaction is responsible for B-cell acute lymphoblastic leukemia caused by JAK2 R683G(S) mutations.PMID 23452118Read ↗

The effects of R683S (G) genetic mutations on the JAK2 activity, structure and stability.Semantic proximity Read ↗

Effects of the I682F mutation on JAK2's activity, structure and stability.Semantic proximity Read ↗

Molecular basis of JAK2 H608Y and H608N mutations in the pathology of acute myeloid leukemia.Semantic proximity Read ↗

Janus Kinases in LeukemiaSemantic proximity Read ↗

Ab initio modeling and experimental assessment of Janus Kinase 2 (JAK2) kinase-pseudokinase complex structure.Semantic proximity Read ↗

Effects of JAK2 V556F mutation on the JAK2's activity, structural stability and the transformation of Ba/F3 cells.Semantic proximity Read ↗

JAK3 Y841 Autophosphorylation Is Critical for STAT5B Activation, Kinase Domain Stability and Dimer FormationSemantic proximity Read ↗

Mechanisms of constitutive activation of Janus kinase 2-V617F revealed at the atomic level through molecular dynamics simulations.Semantic proximity Read ↗

The use of structural biology in Janus kinase targeted drug discovery.Semantic proximity Read ↗

A novel approach to study multi-domain motions in JAK1's activation mechanism based on energy landscape.Semantic proximity Read ↗

Identification of mutant alleles of JAK3 in pediatric patients with acute lymphoblastic leukemia.Semantic proximity Read ↗

Activating mutations of STAT5B and STAT3 in lymphomas derived from γδ-T or NK cells.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.