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Last update 08 May 2025

SLITRK2

Last update 08 May 2025

Basic Info

Synonyms

CXorf1, CXorf2, KIAA1854

+ [5]

Introduction

It is involved in synaptogenesis and promotes excitatory synapse differentiation (PubMed:27273464, PubMed:27812321, PubMed:35840571). Suppresses neurite outgrowth (By similarity). Involved in the negative regulation of NTRK2 (PubMed:35840571).

Drugs associated with SLITRK2

HG-1425

Target

SLITRK2

Mechanism

SLITRK2 modulators

Active Org.-

Originator Org.

Human Genome Sciences, Inc.

Active Indication-

Inactive Indication

Neoplasms

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with SLITRK2

100 Translational Medicine associated with SLITRK2

0 Patents (Medical) associated with SLITRK2

Literatures (Medical) associated with SLITRK2

01 Jan 2023·PeerJ

Transcriptome analysis reveals genes associated with wool fineness in merinos.

Article

Author: Zhao, Zhiwen ; Tian, Yuezhen ; Huang, Xixia ; Wu, Cuiling ; Ma, Shengchao ; Long, Li ; Tian, Kechuan

Hair/wool usually plays an important role in maintaining animal physiological activities, and the economic value of wool cannot be ignored. At present, people set higher demands on wool fineness. Hence, improving wool fineness is the concern of fine wool sheep breeding. Using RNA-Seq to screen the potential candidate genes that associate with wool fineness can provide theoretical references for fine-wool sheep breeding, and also provide us new ideas for further understand the molecular regulation mechanism of hair growth. In this study, we compared the expression pattern difference of genome-wide genes between the skin transcriptomes of Subo and Chinese Merinos. The results showed that, 16 candidate differentially expressed genes (DEGs) (Included: CACNA1S, GP5, LOC101102392, HSF5, SLITRK2, LOC101104661, CREB3L4, COL1A1, PTPRR, SFRP4, LOC443220, COL6A6, COL6A5, LAMA1, LOC114115342 and LOC101116863 genes) that may associate with wool fineness were screened, and these genes were located in signaling pathways that regulate hair follicle development, cycle or hair growth. It is worth noting that, among the 16 DEGs, COL1A1 gene has the highest expression level in Merino skins, and the fold change of LOC101116863 gene is the highest, and the structures of these two genes are both highly conserved in different species. In conclusion, we speculate that these two genes may play a key role in regulating wool fineness and respectively have similar and conserved functions in different species.

01 Jul 2022·iScience

Slitrk2 deficiency causes hyperactivity with altered vestibular function and serotonergic dysregulation

Article

Author: Akagi, Takumi ; Corbett, Danielle ; Yamada, Kazuyuki ; Matsunaga, Hayato ; Matsumoto, Yoshifumi ; Katayama, Kei-Ichi ; Aruga, Jun ; Okamoto, Takehito ; Nagao, Soichi ; Fujita, Wakako ; Kobayashi, Katsunori ; Morimura, Naoko ; Ornthanalai, Veravej G ; Murphy, Niall P ; Hashikawa, Tsutomu

SLITRK2 encodes a transmembrane protein that modulates neurite outgrowth and synaptic activities and is implicated in bipolar disorder. Here, we addressed its physiological roles in mice. In the brain, the Slitrk2 protein was strongly detected in the hippocampus, vestibulocerebellum, and precerebellar nuclei-the vestibular-cerebellar-brainstem neural network including pontine gray and tegmental reticular nucleus. Slitrk2 knockout (KO) mice exhibited increased locomotor activity in novel environments, antidepressant-like behaviors, enhanced vestibular function, and increased plasticity at mossy fiber-CA3 synapses with reduced sensitivity to serotonin. A serotonin metabolite was increased in the hippocampus and amygdala, and serotonergic neurons in the raphe nuclei were decreased in Slitrk2 KO mice. When KO mice were treated with methylphenidate, lithium, or fluoxetine, the mood stabilizer lithium showed a genotype-dependent effect. Taken together, Slitrk2 deficiency causes aberrant neural network activity, synaptic integrity, vestibular function, and serotonergic function, providing molecular-neurophysiological insight into the brain dysregulation in bipolar disorders.

01 Jan 2022·Iranian journal of child neurology

Understanding the Molecular Basis of Fragile X Syndrome Using Differentiated Mesenchymal Stem Cells.

Article

Author: Najmabadi, Hossein ; Ghaderian, Sayyed Mohammad Hossein ; Fazeli, Zahra ; Omrani, Mir Davood

OBJECTIVESFragile X syndrome (FXS) has been known as the most common cause of inherited intellectual disability and autism. This disease results from the loss of fragile X mental retardation protein expression due to the expansion of CGG repeats located on the 5' untranslated region of the fragile X mental retardation 1 (FMR1) gene.MATERIALS & METHODSIn the present study, the peripheral blood-mesenchymal stem cells (PB-MSCs) of two female full mutation carriers were differentiated into neuronal cells by the suppression of bone morphogenesis pathway signaling. Then, the expression of genes adjacent to CGG repeats expansion, including SLIT and NTRK-like protein 2 (SLITRK2), SLIT and NTRK-like protein 4 (SLITRK4), methyl CpG binding protein 2 (MECP2), and gamma-aminobutyric acid receptor subunit alpha-3 (GABRA3), were evaluated in these cells using SYBR Green real-time polymerase chain reaction.RESULTSThe obtained results indicated that the expression of SLITRK2 and SLITRK4 were upregulated and downregulated in the neuron-like cells differentiated from the PB-MSCs of females with FMR1 full mutation, compared to that of the normal females, respectively. Furthermore, the expression of MECP2 and GABRA3 genes were observed to be related to the phenotypic differences observed in the female FMR1 full mutation carriers.CONCLUSIONThe observed association of expression of genes located upstream of the FMR1 gene with phenotypic differences in the female carriers could increase the understanding of novel therapeutic targets for patients with mild symptoms of FXS and the patients affected by other FMR1-related disorders.

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SLITRK2

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