CALB2

Last update 08 May 2025

Basic Info

Synonyms

29 kDa calbindin, CAB29, CAL2

+ [4]

Introduction

Calretinin is a calcium-binding protein which is abundant in auditory neurons.

100 Clinical Results associated with CALB2

100 Translational Medicine associated with CALB2

0 Patents (Medical) associated with CALB2

4,030

Literatures (Medical) associated with CALB2

01 Jun 2025·Molecular and Cellular Neuroscience

Olfactory bulb interneurons – The developmental timeline and targeting defined by embryonic neurogenesis

Article

Author: Martin-Lopez, Eduardo ; Greer, Charles A ; Spence, Natalie J ; Brennan, Bowen ; Lefèvre, Marion ; Lange, Nathaniel W ; Han, Kimberly

The generation of mouse olfactory bulb (OB) interneurons (INs) is initiated in the embryo but continues throughout life. It is generally agreed that OB INs generated postnatally affect the connectivity of the OB, depending on the timeline of neurogenesis. Here, we focused on OB INs generated embryonically, which have generally received less attention than those generated in the adult. Birthdates of embryonic INs were differentiated by maternal injections of thymidine analogs and their final destinations and phenotypes in the OB analyzed by immunohistochemistry. We found that the first embryonic INs were generated at embryonic day 10 (E10) and continued through the entire embryonic development. Analysis in adult tissues showed that embryonic INs were retained and were distributed across all layers of the OB. Interestingly, an initial lateral preference in cell density was seen in INs generated during E11-E13. Although INs are broadly distributed in the OB, we found that within the granule cell layer (GCL), OB INs distributed mostly in the superficial GCL. Immunostaining for calbindin, parvalbumin, tyrosine hydroxylase, 5T4 and calretinin were lacking co-expression with thymidine analogs labeled cells, suggesting that maturation of embryonic INs occurred slowly following birth. We studied the embryonic neuroblasts migration and differentiation by labeling IN progenitor cells in the lateral ganglionic eminence using in utero electroporation. We found that IN neuroblasts reached the primordial OB as early as E13 and began to differentiate apical dendrites by E15, which extended into the developing external plexiform layer. We established E16 as the embryonic stage at which the prototypical chain of migrating neuroblasts denoting the embryonic rostral migratory stream (RMS) was visible. Collectively, our data highlight the importance of studying OB INs in isolated time windows to better understand the formation of circuits that define the olfactory system function.

01 May 2025·Pain

Spinal lumbar Urocortin 3-expressing neurons are associated with both scratching and Compound 48/80-induced sensations

Article

Author: Ceder, Mikaela M. ; Lagerström, Malin C. ; Weman, Hannah M. ; Öhman-Mägi, Caroline ; Ahemaiti, Aikeremu ; Bengtsson, Erica ; Magnusson, Kajsa A. ; Henriksson, Katharina ; Franck, Marina C. M. ; Koning, Harmen K.

AbstractUrocortin 3 is a neuropeptide that belongs to the corticotropin-releasing hormone family and is involved in mechanosensation and stress regulation. In this study, we show that Urocortin 3 marks a population of excitatory neurons in the mouse spinal cord, divided into 2 nonoverlapping subpopulations expressing protein kinase C gamma or calretinin/calbindin 2, populations previously associated with mechanosensation. Electrophysiological experiments demonstrated that lumbar spinal Urocortin 3 neurons receive both glycinergic and GABAergic local tonic inhibition, and monosynaptic inputs from both Aβ and C fibers, which could be confirmed by retrograde trans-synaptic rabies tracing. Furthermore, fos analyses showed that subpopulations of lumbar Urocortin 3 neurons are activated by artificial scratching or Compound 48/80-induced sensations. Chemogenetic activation of lumbar Urocortin 3-Cre neurons evoked a targeted biting/licking behavior towards the corresponding dermatome and chemogenetic inhibition decreased Compound 48/80-induced behavior. Hence, spinal lumbar Urocortin 3 neurons represent a mechanically associated population with roles in both scratching and Compound 48/80-induced sensations.

01 Apr 2025·Thoracic Cancer

Cytoplasmic HuR Expression Enhances Chemoresistance in Pleural Mesothelioma Through Increased Expression of CALB2, Promotion of the E2F Pathway, and Suppression of the p53 Pathway

Article

Author: Okubo, Kenichi ; Taniguchi, Yusuke ; Sugita, Keisuke ; Kurata, Morito ; Ishibashi, Hironori ; Kirimura, Susumu ; Kinowaki, Yuko

ABSTRACTIntroductionChemotherapy is crucial for treating pleural mesothelioma; however, the outcomes are poor, necessitating an urgent need to study the mechanism of chemotherapy resistance in mesothelioma cells. Human antigen R (HuR), an RNA‐binding protein and key post‐transcriptional regulator of mRNA, is linked to poor prognosis in cancers like mesothelioma. We investigated the involvement of cytoplasmic HuR expression in drug resistance mechanisms in mesothelioma.MethodsWe retrospectively evaluated cytoplasmic HuR expression in 30 patients with pleural mesothelioma who underwent surgical resection using immunohistochemistry. We also examined the role of forced cytoplasmic expression of HuR in drug resistance using mesothelioma cell lines and performed RNA‐Seq analysis to identify gene expression changes responsible for drug resistance acquisition via HuR cytoplasmic expression.ResultsPatients with mesotheliomas who expressed cytoplasmic HuR exhibited significantly worse disease‐free survival following post‐operative chemotherapy. Forced cytoplasmic HuR expression in mesothelioma cell lines increased chemotherapy resistance through increased expression of CALB2, upregulation of the E2F pathway and suppression of the p53 pathway.ConclusionsCytoplasmic HuR expression increases the chemoresistance and postoperative recurrence risk of pleural mesothelioma, making it a potential biomarker for predicting therapeutic prognosis. However, the mechanism of HuR transfer to the cytoplasm remains unclear for therapeutic application.

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CALB2

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