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1.
Cell Death Dis ; 11(6): 468, 2020 Jun 17.
Artigo em Inglês | MEDLINE | ID: mdl-32555216

RESUMO

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

2.
Genes (Basel) ; 11(3)2020 03 11.
Artigo em Inglês | MEDLINE | ID: mdl-32168764

RESUMO

Hair growth and morphology are generally regulated by the hair cycle in mammals. Fibroblast Growth Factor 5 (FGF5), which is a hair cycle regulator, has a role in regulating the hair cycle during the transition from the anagen phase to the catagen phase, and a hereditary long hair phenotype has been widely reported when FGF5 is mutated in humans and other species. However, there has been no such report in rabbits. Thus, the first exon of rabbit FGF5 was disrupted by the CRISPR/Cas9 system, and the phenotype of FGF5-/- rabbits was characterized while using hematoxylin and eosin (H&E) staining, immunohistochemistry, quantitative PCR, scanning electron microscopy, and western blotting. The results showed a significant and systemic long hair phenotype in the FGF5-/- rabbits, which indicated that FGF5 is a negative regulator of hair growth. In addition, a decreased diameter of the fiber and a higher area proportion of hair follicle clusters were determined in FGF5-/- rabbits as compared with the WT rabbits. Further investigation verified that prolonging the anagen phase in rabbits, with decreased BMP2/4 pathway signaling and increased VERSICAN pathway signaling, caused the systemic long hair phenotype. Taken together, these results indicate a systemic long hair phenotype by prolonging anagen in FGF5-/- rabbits, which could be widely used for Fur production and an ideal model for studying the mechanism of long hair in the future.

3.
RNA Biol ; 17(5): 623-629, 2020 May.
Artigo em Inglês | MEDLINE | ID: mdl-32036747

RESUMO

The previous report shows the minimal promoter (P1) contributes to the Xist RNA activation in cells, while the role of the Xist P1 has not yet been investigated in animal individuals. Here, female Xist P1 knockout rabbits (Xist P1-/-) were generated for the studies. The results showed that there is no significant difference in transmission ratio, Xist and X-linked genes expression, and Xist RNA localization between the female wild type (WT) and Xist P1-/- rabbits, suggesting that P1 is non-essential for Xist expression and XCI in rabbits. Our study has explored the function of Xist P1 in animal level for the first time, and the results provide new ideas for future studies of XCI mechanisms.

4.
FASEB J ; 34(1): 588-596, 2020 01.
Artigo em Inglês | MEDLINE | ID: mdl-31914687

RESUMO

Base editors, composed of a cytidine deaminase or an evolved adenine deaminase fused to Cas9 nickase, enable efficient C-to-T or A-to-G conversion in various organisms. However, the NGG protospacer adjacent motif (PAM) requirement of Streptococcus pyogenes Cas9 (SpCas9) substantially limits the target sites suitable for base editing. Quite recently, a new engineered SpCas9-NG variant, which can recognize minimal NG PAMs more efficiently than the present xCas9 variant. Here, we investigated the efficiency and PAM compatibility of SpCas9-NG-assisted cytidine base editors (CBEs) and adenine base editors (ABEs) in rabbits. In this study, we showed that NG-BE4max and NG-ABEmax systems can achieve a targeted mutation efficiency of 75%-100% and 80%-100% with excellent PAM compatibility of NGN PAMs in rabbit embryos, respectively. In addition, both base editors were successfully applied to create new rabbit models with precise point mutations, demonstrating their high efficiency and expanded genome-targeting scope in rabbits. Meanwhile, NG-ABEmax can be used to precisely mimic human Hoxc13 p.Q271R missense mutation in Founder (F0) rabbits, which is arduous for conventional ABEs to achieve due to a NGA PAM requirement. Collectively, NG-BE4max and NG-ABEmax systems provide promising tools to perform efficient base editing with expanded targeting scope in rabbits and enhances its capacity to model human diseases.

5.
Cell Death Dis ; 11(1): 36, 2020 01 20.
Artigo em Inglês | MEDLINE | ID: mdl-31959743

RESUMO

Cytidine base editors, composed of a cytidine deaminase fused to Cas9 nickase, enable efficient C-to-T conversion in various organisms. However, current base editors suffer from severe trade-off between editing efficiency and precision. Here, based on rationally mutated cytidine deaminase domain, we develop a new base editor, YFE-BE4max, effectively narrow the editing width to as little as approximately three nucleotides while maintaining high efficiency in rabbits. Moreover, YFE-BE4max successfully mediated the Tyr p. Q68Stop and Lmna p. G607G mutation in F0 rabbit with high efficiency and precision, which precisely recapitulates the pathological features of human OCA1 and HGPS, respectively. Collectively, YFE-BE4max system provide promising tools to perform efficient base editing with high precision in rabbits and enhances its capacity to precisely model human diseases.

7.
Cell Mol Life Sci ; 2019 Nov 13.
Artigo em Inglês | MEDLINE | ID: mdl-31720743

RESUMO

Glucokinase (GCK) is a key enzyme in glucose sensing and glycemic regulation. In humans, mutations in the GCK gene cause maturity-onset diabetes of the young 2 (MODY-2), a disease that is characterized by an early-onset and persistent hyperglycemia. It is known that Gck knockout (KO) is lethal in mice with Gck KO mice dying within 2 weeks after birth. Therefore, Gck KO mice are not suitable for preclinical study and have limited suitability to study the pathophysiological role of glucokinase in vivo. Here, we report the generation of a novel rabbit with a non-frameshift mutation of GCK gene (GCK-NFS) by cytoplasm microinjection of Cas9 mRNA and gRNA. These GCK-NFS rabbits showed typical features of MODY-2 including hyperglycemia and glucose intolerance with similar survival rate and weight compared to wild-type (WT) rabbits. The diabetic phenotype including pancreatic and renal dysfunction was also found in the F1-generation rabbits, indicating that the genetic modification is germline transmissible. Treatment of GCK-NFS rabbit with glimepiride successfully reduced the fasting blood glucose drastically and improved its islet function. In conclusion, this novel GCK mutant rabbit generated with the CRISPR/Cas9 system mimics most, if not all, histopathological and functional defects seen in MODY-2 patients such as hyperglycemia and will be a valuable rabbit model for preclinical studies and drug screening for diabetes as well as for studying the pathophysiological role of glucokinase.

8.
Int J Mol Med ; 44(3): 1063-1077, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31524221

RESUMO

Epithelial cell adhesion molecule (EpCAM) is highly expressed during liver development and carcinogenesis, However, its functions and underlying mechanisms remain unclear. Clustered regularly interspaced short palindromic repeats (CRISPRs)/CRISPR­associated protein 9 (Cas9) technology was used in the current study to establish EpCAM­/­ mice. The expression of EpCAM in the livers of the mice at embryonic day (E)18.5 and post­natal day (P)0 was detected by immunofluorescence staining. The expression of genes associated with the development and glycogen metabolism was also assessed by reverse transcription­quantitative PCR. Additionally, the liver tissue of the EpCAM­/­ and wild­type mice was used for non­coding RNA sequencing. The results of RNA sequencing revealed 11 up­regulated and 12 downregulated circular RNAs (circRNAs). Kyoto Encyclopedia of Genes and Genomes analysis for resource genes determined that the top altered pathways included cell junctions, cell cycle, immune signaling and metabolism. This analysis was also utilized to predict the target association of the circRNA­microRNA­mRNA network. The comprehensive liver tissue circRNA expression profiles produced in the present study may help to elucidate the functions and mechanisms of EpCAM during liver development.


Assuntos
Biomarcadores , Molécula de Adesão da Célula Epitelial/deficiência , Fígado/metabolismo , RNA Circular , Animais , Sequência de Bases , Biologia Computacional/métodos , Molécula de Adesão da Célula Epitelial/química , Molécula de Adesão da Célula Epitelial/genética , Perfilação da Expressão Gênica , Ontologia Genética , Redes Reguladoras de Genes , Genótipo , Camundongos , Camundongos Knockout , MicroRNAs/genética , Fenótipo , RNA Mensageiro/genética , Reprodutibilidade dos Testes
9.
Nat Commun ; 10(1): 2852, 2019 06 28.
Artigo em Inglês | MEDLINE | ID: mdl-31253764

RESUMO

Cytosine base editors (CBEs) enable programmable C-to-T conversion without DNA double-stranded breaks and homology-directed repair in a variety of organisms, which exhibit great potential for agricultural and biomedical applications. However, all reported cases only involved C-to-T substitution at a single targeted genomic site. Whether C-to-T substitution is effective in multiple sites/loci has not been verified in large animals. Here, by using pigs, an important animal for agriculture and biomedicine, as the subjective animal, we showed that CBEs could efficiently induce C-to-T conversions at multiple sites/loci with the combination of three genes, including DMD, TYR, and LMNA, or RAG1, RAG2, and IL2RG, simultaneously, at the embryonic and cellular levels. CBEs also could disrupt genes (pol gene of porcine endogenous retrovirus) with dozens of copies by introducing multiple premature stop codons. With the CBEs, pigs carrying single gene or multiple gene point mutations were generated through embryo injection or nuclear transfer approach.


Assuntos
Sistemas CRISPR-Cas , Edição de Genes , Mutação Puntual , Suínos/genética , Desaminase APOBEC-1 , Animais , Sequência de Bases , Proteína 9 Associada à CRISPR , DNA/genética , Técnicas de Cultura Embrionária , Embrião de Mamíferos , Genoma , Técnicas de Transferência Nuclear/veterinária , RNA Guia/metabolismo , RNA Mensageiro/genética , RNA Mensageiro/metabolismo
10.
Nat Cell Biol ; 21(6): 687-699, 2019 06.
Artigo em Inglês | MEDLINE | ID: mdl-31160711

RESUMO

We recently derived mouse expanded potential stem cells (EPSCs) from individual blastomeres by inhibiting the critical molecular pathways that predispose their differentiation. EPSCs had enriched molecular signatures of blastomeres and possessed developmental potency for all embryonic and extra-embryonic cell lineages. Here, we report the derivation of porcine EPSCs, which express key pluripotency genes, are genetically stable, permit genome editing, differentiate to derivatives of the three germ layers in chimeras and produce primordial germ cell-like cells in vitro. Under similar conditions, human embryonic stem cells and induced pluripotent stem cells can be converted, or somatic cells directly reprogrammed, to EPSCs that display the molecular and functional attributes reminiscent of porcine EPSCs. Importantly, trophoblast stem-cell-like cells can be generated from both human and porcine EPSCs. Our pathway-inhibition paradigm thus opens an avenue for generating mammalian pluripotent stem cells, and EPSCs present a unique cellular platform for translational research in biotechnology and regenerative medicine.


Assuntos
Diferenciação Celular/genética , Reprogramação Celular/genética , Células-Tronco Pluripotentes Induzidas/citologia , Células-Tronco Pluripotentes/citologia , Animais , Blastômeros/citologia , Blastômeros/metabolismo , Linhagem da Célula/genética , Células-Tronco Embrionárias/citologia , Camadas Germinativas/crescimento & desenvolvimento , Camadas Germinativas/metabolismo , Humanos , Camundongos , Medicina Regenerativa , Transdução de Sinais/genética , Suínos , Trofoblastos/citologia , Trofoblastos/metabolismo
11.
Biochim Biophys Acta Mol Basis Dis ; 1865(9): 2356-2367, 2019 09 01.
Artigo em Inglês | MEDLINE | ID: mdl-31150757

RESUMO

The cleft lip with or without cleft palate (CL/P) is one of the most common congenital defects in humans. Genome-wide association studies (GWAS) have been widely used for identifying candidate genes, and different genes or chromosomal regions have shown strong evidence for the presence of causal genes in CL/P. To date, two independent GWAS have identified GADD45G as influencing risk for CL/P. However, there is no animal model evidence about GADD45G related to CL/P. Here, we reported the generation of a novel GADD45G mutated rabbit model by CRISPR/Cas9 and CRISPR-based BE4-Gam systems. The homozygous (GADD45G-/-) while not heterozygous (GADD45G+/-) pups died after birth due to severe craniofacial defects of unilateral or bilateral cleft lip (CL). Moreover, the disorder of proliferation, apoptosis and epithelial-mesenchymal transition (EMT) were also determined in the medial and lateral nasal processes (MNP and LNP) of the embryonic day 13 (E13) GADD45G-/- rabbits, which compared with the normal wild type (WT) rabbits. Thus, our study confirmed for the first time that loss of GADD45G lead to CL at the animal level and provided new insights into the crucial role of GADD45G for upper lip formation and fusion.


Assuntos
Fenda Labial/patologia , Peptídeos e Proteínas de Sinalização Intracelular/genética , Animais , Apoptose , Sistemas CRISPR-Cas/genética , Proliferação de Células , Fenda Labial/genética , Fenda Labial/veterinária , Embrião de Mamíferos/citologia , Embrião de Mamíferos/metabolismo , Embrião de Mamíferos/patologia , Desenvolvimento Embrionário , Transição Epitelial-Mesenquimal , Técnicas de Inativação de Genes/métodos , Homozigoto , Peptídeos e Proteínas de Sinalização Intracelular/química , Peptídeos e Proteínas de Sinalização Intracelular/metabolismo , Lábio/patologia , Mutação , Estrutura Terciária de Proteína , Coelhos
14.
FASEB J ; 33(8): 9210-9219, 2019 08.
Artigo em Inglês | MEDLINE | ID: mdl-31071267

RESUMO

Cytidine base editors, which are composed of a cytidine deaminase fused to clustered regularly interspaced short palindromic repeat (CRISPR)-associated protein 9 (Cas9) nickase, enable the efficient conversion of the C·G base pair to T·A in various organisms. However, the currently used rat apolipoprotein B mRNA-editing enzyme, catalytic polypeptide 1(rA1)-based BE3 is often inefficient in target Cs that are immediately downstream of a G (GC context). Here, we observed that, with an 11-nt editing window, an optimized activation-induced cytidine deaminase (AID)-Cas9 fusion can efficiently convert C to T in a variety of sequence contexts in rabbits. Strikingly, the enhanced AID-Cas9 fusion (eAID-BE4max) has significant effectiveness of inducing Tyr p.R299H mutation in GC contexts (from 16.67 to 83.33%) in comparison with BE3 in founder rabbits. Furthermore, the engineered AID-Cas9 variants were produced with reduced bystander activity [eAID (N51G)-BE4max] and increased genome-targeting scope (eAID-NG-BE4max). Overall, this work provides a series of improved tools that were generated using optimized AID-Cas9 fusions and associated engineered variants that can be used for efficient and versatile C-to-T base editing, especially in GC contexts.-Liu, Z., Shan, H., Chen, S., Chen, M., Zhang, Q., Lai, L., Li, Z. Improved base editor for efficient editing in GC contexts in rabbits with an optimized AID-Cas9 fusion.

15.
Nat Commun ; 10(1): 1817, 2019 04 18.
Artigo em Inglês | MEDLINE | ID: mdl-31000720

RESUMO

Neurodegenerative diseases like Alzheimer's disease, Parkinson's disease and Huntington's disease manifest with the neuronal accumulation of toxic proteins. Since autophagy upregulation enhances the clearance of such proteins and ameliorates their toxicities in animal models, we and others have sought to re-position/re-profile existing compounds used in humans to identify those that may induce autophagy in the brain. A key challenge with this approach is to assess if any hits identified can induce neuronal autophagy at concentrations that would be seen in humans taking the drug for its conventional indication. Here we report that felodipine, an L-type calcium channel blocker and anti-hypertensive drug, induces autophagy and clears diverse aggregate-prone, neurodegenerative disease-associated proteins. Felodipine can clear mutant α-synuclein in mouse brains at plasma concentrations similar to those that would be seen in humans taking the drug. This is associated with neuroprotection in mice, suggesting the promise of this compound for use in neurodegeneration.


Assuntos
Autofagia/efeitos dos fármacos , Reposicionamento de Medicamentos , Felodipino/farmacologia , Doenças Neurodegenerativas/tratamento farmacológico , Fármacos Neuroprotetores/farmacologia , Animais , Animais Geneticamente Modificados , Linhagem Celular , Córtex Cerebral/citologia , Córtex Cerebral/patologia , Modelos Animais de Doenças , Embrião de Mamíferos , Embrião não Mamífero , Felodipino/uso terapêutico , Feminino , Humanos , Células-Tronco Pluripotentes Induzidas , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Mutação , Doenças Neurodegenerativas/genética , Doenças Neurodegenerativas/patologia , Neurônios/efeitos dos fármacos , Neurônios/patologia , Fármacos Neuroprotetores/uso terapêutico , Cultura Primária de Células , Suínos , Porco Miniatura , Resultado do Tratamento , Peixe-Zebra , alfa-Sinucleína/genética , alfa-Sinucleína/metabolismo
16.
Cell Mol Life Sci ; 76(20): 4155-4164, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31030226

RESUMO

Evolved xCas9(3.7) variant with broad PAM compatibility has been reported in cell lines, while its editing efficiency was site-specific. Here, we show that xCas9(3.7) can recognize a broad PAMs including NGG, NGA, and NGT, in both embryos and Founder (F0) rabbits. Furthermore, the codon-optimized xCas9-derived base editors, exBE4 and exABE, can dramatically improve the base editing efficiencies in rabbit embryos. Our results demonstrated that the optimized xCas9 with expanded PAM compatibility and enhanced base editing efficiency could be used for precise gene modifications in organisms.


Assuntos
Proteína 9 Associada à CRISPR/genética , Sistemas CRISPR-Cas , Efeito Fundador , Edição de Genes/métodos , Marcação de Genes/métodos , RNA Guia/genética , Animais , Animais Geneticamente Modificados , Proteína 9 Associada à CRISPR/metabolismo , Códon , Distrofina/genética , Distrofina/metabolismo , Embrião de Mamíferos , Expressão Gênica , Sequenciamento de Nucleotídeos em Larga Escala , Microinjeções , Plasmídeos/química , Plasmídeos/metabolismo , Proteínas de Ligação a Poli(A)/genética , Proteínas de Ligação a Poli(A)/metabolismo , Presenilina-1/genética , Presenilina-1/metabolismo , RNA Guia/metabolismo , Coelhos , Repetições de Trinucleotídeos , Zigoto
17.
J Gastroenterol Hepatol ; 34(10): 1851-1859, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-30884543

RESUMO

BACKGROUND AND AIM: Bioartificial livers (BALs) are considered as a solution to bridge patients with acute liver failure to liver transplantation or to assist in spontaneous recovery for patients with end-stage liver disease. Pig is the best donor of hepatocytes for BALs in clinical trials, because metabolic and detoxification function of its liver are close to human. However, using pig hepatocytes for BALs remains controversial for safety concern owing to nonhuman proteins secretion. Herein, we attempt to establish modified pigs expressing humanized liver proteins, blood-coagulation factor VII (F7), and albumin (ALB). These pigs should also be porcine endogenous retrovirus subtype C (PERV-C) free so that their ability of transmitting PERV to human could be diminished seriously. METHODS: We devised both homology-dependent and independent knock-in approaches to insert a fusion of hF7 and hALB gene downstream the site of pig endogenous F7 promoter in pig fetal fibroblasts negative for PERV-C. The modified pigs were then generated through somatic cell nuclear transfer. RESULTS: We obtained 14 and 10 cloned pigs by homology-dependent and independent approaches, respectively. Among them, 19 cloned pigs were with expected gene modification and 13 are alive to date. These modified pigs can successfully express hF7 and hALB in the liver and serum, and the expressed hF7 exhibits normal coagulation activity. CONCLUSIONS: The gene-edited pigs expressing hF7 and hALB in the liver were generated successfully. We anticipate that our pigs could provide an alternative cell source for BALs as a promising treatment for patients with acute liver failure.


Assuntos
Fator VII/genética , Fibroblastos/metabolismo , Edição de Genes , Técnicas de Introdução de Genes , Hepatócitos/metabolismo , Fígado Artificial , Albumina Sérica Humana/genética , Sus scrofa/genética , Animais , Animais Geneticamente Modificados , Linhagem Celular , Fator VII/metabolismo , Fibroblastos/transplante , Genótipo , Hepatócitos/transplante , Fenótipo , Albumina Sérica Humana/metabolismo , Transplante Heterólogo
18.
J Bone Miner Res ; 34(6): 1115-1128, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-30827034

RESUMO

DMP1 (dentin matrix protein 1) is an extracellular matrix protein highly expressed in bones. Studies of Dmp1 knockout (KO) mice led to the discovery of a rare autosomal recessive form of hypophosphatemic rickets (ARHR) caused by DMP1 mutations. However, there are limitations for using this mouse model to study ARHR, including a lack of Haversian canals and osteons (that occurs only in large mammalian bones), high levels of fibroblast growth factor 23 (FGF23), and PTH, in comparison with a moderate elevation of FGF23 and unchanged PTH in human ARHR patients. To better understand this rare disease, we deleted the DMP1 gene in rabbit using CRISPR/Cas9. This rabbit model recapitulated many features of human ARHR, such as the rachitic rosary (expansion of the anterior rib ends at the costochondral junctions), moderately increased FGF23, and normal PTH levels, as well as severe defects in bone mineralization. Unexpectedly, all DMP1 KO rabbits died by postnatal week 8. They developed a severe bone microarchitecture defect: a major increase in the central canal areas of osteons, concurrent with massive accumulation of osteoid throughout all bone matrix (a defect in mineralization), suggesting a new paradigm, where rickets is caused by a combination of a defect in bone microarchitecture and a failure in mineralization. Furthermore, a study of DMP1 KO bones found accelerated chondrogenesis, whereas ARHR has commonly been thought to be involved in reduced chondrogenesis. Our findings with newly developed DMP1 KO rabbits suggest a revised understanding of the mechanism underlying ARHR. © 2019 American Society for Bone and Mineral Research.

19.
Aging Dis ; 10(1): 102-115, 2019 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-30705772

RESUMO

Premature aging syndromes are rare genetic disorders mimicking clinical and molecular features of aging. Products of the LMNA gene, primarily lamin A and C, are major components of the nuclear lamina. A recently identified group of premature aging syndromes was related to mutations of the LMNA gene. Although LMNA disorders have been identified in premature aging syndromes, affect specifically the skeletal muscles, cardiac muscles, and lipodystrophy, understanding the pathogenic mechanisms still need to be elucidated. Here, to establish a rabbit knockout (KO) model of premature aging syndromes, we performed precise LMNA targeting in rabbits via co-injection of Cas9/sgRNA mRNA into zygotes. The LMNA-KO rabbits exhibited reduced locomotion activity with abnormal stiff walking posture and a shortened stature, all of them died within 22 days. In addition, cardiomyopathy, muscular dystrophy, bone and joint abnormalities, as well as lipodystrophy were observed in LMNA-KO rabbits. In conclusion, the novel rabbit LMNA-KO model, displayed typical features of histopathological defects that are observed in premature aging syndromes, and may be utilized as a valuable resource for understanding the pathophysiological mechanisms of premature aging syndromes and elucidating mysteries of the normal process of aging in humans.

20.
FASEB J ; 33(1): 1226-1234, 2019 01.
Artigo em Inglês | MEDLINE | ID: mdl-30125135

RESUMO

Pure hair and nail ectodermal dysplasia 9 (ECTD-9) is an autosomal recessive genetic disease caused by mutation of HOXC13 and is characterized by hypotrichosis and nail dystrophy in humans. Unlike patients with ECTD-9, Hoxc13-mutated mice and pigs do not faithfully recapitulate the phenotype of hypotrichosis, so there is a limited understanding of the molecular mechanism of Hoxc13-mediated hypotrichosis in animal models and clinically. Here, the homozygous Hoxc13-/- rabbits showed complete loss of hair on the head and dorsum, whereas hypotrichosis in the limbs and tail were determined in the Hoxc13-/- rabbits. In addition, reduced hair follicles (HFs) while the enlarged and increased number of sebaceous glands (SGs) were also found in the Hoxc13-/- rabbits, showing that the disrupted balance between HFs and SGs may respond to hypotrichosis of ECTD-9 in an animal model and clinically. Therefore, our findings demonstrate that Hoxc13-/- rabbits can be used as a model for human ECTD-9, especially to understand the pathologic mechanism of hypotrichosis. Moreover, the disrupted balance between HFs and SGs, especially in the Hoxc13-/- rabbits, can be used as an ideal animal model for dermatology ailments, such as acne and hypotrichosis, in preclinical studies.-Deng, J., Chen, M., Liu, Z., Song, Y., Sui, T., Lai, L., Li, Z. The disrupted balance between hair follicles and sebaceous glands in Hoxc13-ablated rabbits.


Assuntos
Deleção de Genes , Cabelo/metabolismo , Proteínas de Homeodomínio/genética , Glândulas Sebáceas/metabolismo , Animais , Sistemas CRISPR-Cas , Modelos Animais de Doenças , Displasia Ectodérmica/genética , Hipotricose/congênito , Hipotricose/genética , Mutação , Fenótipo , Coelhos
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