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Last update 08 May 2025

CRK

Last update 08 May 2025

Basic Info

Synonyms

Adapter molecule crk, CRK, CRK proto-oncogene, adaptor protein

+ [2]

Introduction

Regulates cell adhesion, spreading and migration (PubMed:31311869). Mediates attachment-induced MAPK8 activation, membrane ruffling and cell motility in a Rac-dependent manner. Involved in phagocytosis of apoptotic cells and cell motility via its interaction with DOCK1 and DOCK4 (PubMed:19004829). May regulate the EFNA5-EPHA3 signaling (By similarity). Involved in cell branching and adhesion mediated by BCAR1-CRK-RAPGEF1 signaling and activation of RAP1.

Drugs associated with CRK

RGB-286147

Target

CDK x CRK

Mechanism

CDK inhibitors [+1]

Active Org.

ThinkMolecular Technologies Pvt. Ltd

Originator Org.

ThinkMolecular Technologies Pvt. Ltd

Active Indication-

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

CN119013271

Patent Mining

Target

CRK x CRKL

Mechanism

CRK inhibitors

Active Org.

Rutgers State University of New Jersey

Originator Org.

Rutgers State University of New Jersey

Active Indication

Neoplasms [+1]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with CRK

100 Translational Medicine associated with CRK

0 Patents (Medical) associated with CRK

892

Literatures (Medical) associated with CRK

01 Mar 2025·American Journal of Medical Genetics Part A

Ring Chromosome 17 Syndrome—A Case Report and Discussion of Diagnostic Methods

Article

Author: Kim, Sun Young ; Kossoff, Eric ; Sadreameli, Christy ; Wohler, Elizabeth ; Gutierrez, Maria Jimena ; Sobreira, Nara Lygia

ABSTRACTRing chromosome 17 and 17p13.3 deletion syndrome are phenotypically heterogeneous diseases with similar clinical features. The ring chromosome 17 phenotypic features range from the Miller–Dieker syndrome characterized by deletion of the PAFAH1B1 gene, lissencephaly, hypotonia, dysphagia, café au lait spots, and severe intellectual disability, to a milder phenotype characterized by microcephaly, seizures, delayed development, minor facial dysmorphic features, clinodactyly, short stature, café au lait spots, retinal flecking, and deletion of the YWHAE and CRK genes. Similarly, the phenotypic features of the 17p13.3 deletion syndrome range from the Miller–Dieker syndrome caused by loss of function of the PAFAH1B1 gene and characterized by lissencephaly, microcephaly, seizures, hypotonia, and severe intellectual disability to a milder phenotype characterized by nonspecific white matter changes, microcephaly, seizures, delayed development, short stature, and deletion of the YWHAE and CRK genes. Café au lait spots and retinal or axillary freckling have been noted in the ring chromosome 17 syndrome but not in 17p13.3 deletion syndrome. We report a 5‐year‐old girl with a history of intrauterine growth retardation, short stature, intractable epilepsy, expressive language disorder, clinodactyly, multiple café au lait spots, and retinal freckling who was initially diagnosed with 17p13.3 deletion syndrome involving YWHAE and CRK but not PAFAH1B1 on CGH array. However, cytogenetic analysis of G‐banded chromosomes revealed mosaic ring chromosome 17. Optical genome mapping simultaneously identified the 17p13.3 deletion and the mosaic ring chromosome 17. This case report highlights the limitations of the arrays and sequencing methods for identifying structural variants, the need to investigate further deletions and duplications identified by arrays, mainly considering atypical phenotypic features, and suggests that OGM could be used as a first‐tier test with exome sequencing for the diagnosis of patients with dysmorphic features, intellectual disability, and seizure disorder.

01 Mar 2025·Cell Death & Differentiation

SLAMF7 (CD319) on activated CD8+ T cells transduces environmental cues to initiate cytotoxic effector cell responses

Article

Author: Lingel, Holger ; Fischer, Laura ; Arra, Aditya ; Han, Irina ; Freund, Christian ; Kuropka, Benno ; Brunner-Weinzierl, Monika C ; Remstedt, Sven ; Sander, Jan-Erik ; Philipsen, Lars

AbstractCD8+ T-cell responses are meticulously orchestrated processes regulated by intercellular receptor:ligand interactions. These interactions critically control the dynamics of CD8+ T-cell populations that is crucial to overcome threats such as viral infections or cancer. Yet, the mechanisms governing these dynamics remain incompletely elucidated. Here, we identified a hitherto unknown T-cell referred function of the self-ligating surface receptor SLAMF7 (CD319) on CD8+ T cells during initiation of cytotoxic T-cell responses. According to its cytotoxicity related expression on T effector cells, we found that CD8+ T cells could utilize SLAMF7 to transduce environmental cues into cellular interactions and information exchange. Indeed, SLAMF7 facilitated a dose-dependent formation of stable homotypic contacts that ultimately resulted in stable cell-contacts, quorum populations and commitment to expansion and differentiation. Using pull-down assays and network analyses, we identified novel SLAMF7-binding intracellular signaling molecules including the CRK, CRKL, and Nck adaptors, which are involved in T-cell contact formation and may mediate SLAMF7 functions in sensing and adhesion. Hence, providing SLAMF7 signals during antigen recognition of CD8+ T cells enhanced their overall magnitude, particularly in responses towards low-affinity antigens, resulting in a significant boost in their proliferation and cytotoxic capacity. Overall, we have identified and characterized a potent initiator of the cytotoxic T lymphocyte response program and revealed advanced mechanisms to improve CD8+ T-cell response decisions against weak viral or tumor-associated antigens, thereby strengthening our defense against such adversaries.

01 Jan 2025·Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics

Identification of dystrophin Dp71dΔ71-associated proteins in PC12 cells by quantitative proteomics

Article

Author: Ríos-Castro, Emmanuel ; Azotla-Vilchis, Coztli ; Aragón, Jorge ; Ceja, Víctor ; Merino-Jiménez, Candelaria ; Montanez, Cecilia

Dystrophin Dp71 is essential for the development of the nervous system. Its alteration is associated with intellectual disability. Different Dp71 isoforms are generated by alternative splicing; however, their functions have not been fully described. Here, we identified Dp71d_Δ71-associated proteins to understand the complex functions. PC12 cells, stably transfected with pTRE2pur-Myc/Dp71d_Δ71 or pTRE2pur-Myc empty vector (EV), were analyzed by immunoprecipitation followed with quantitative proteomics with data-independent acquisition and ion mobility separation. We used the Top3 method to quantify absolutely every protein detected. A total of 106 proteins were quantified with Progenesis QI software and the database UP000002494. Seven new proteins associated with Dp71d_Δ71 were selected with at least 2-fold quantity between immunoprecipitated proteins of PC12-Myc/Dp71d_Δ71 versus PC12-EV cells. These results revealed new proteins that interact with Dp71d_Δ71, including β-Tubulin, S-adenosylmethionine synthase isoform type-2, adapter molecule crk, helicase with zinc finger 2, WD repeat domain 93, cyclin-L2 and myosin-10, which are related to cell migration and/or cell growth. The results lay the foundation for future research on the relationship between these proteins and Dp71 isoforms.

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CRK

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