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BIOCA Team > 5. Proteinas Fibrosas > Flashcards

5. Proteinas Fibrosas Flashcards

1
Q

Proteina fibrosa

A

Combinacion de elementos de estructura secundaria

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2
Q

Tres polipeptidos de cadena α

A

Colageno

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3
Q

Tipos de colageno

A

25

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4
Q

Las cadenas polipeptidas se unen por

A

Puentes de hidrogeno intercatenarios

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5
Q

Colageno tipo I

A

α12,α2

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6
Q

Colageno tipo II

A

α13

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7
Q

Formadores de fibrillas

A

I, II y III

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8
Q

Colageno tipo III en

A

Capilares

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9
Q

Formadores de redes

A

Tipo IV y VIII

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10
Q

Relacionados a fibrillas

A

IX y XII

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11
Q

Colageno rico en

A

Prolina y glicina

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12
Q

Glicina se encuentra en

A

Cada 3era posición

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13
Q

Aminoacidos no extandar

A

Hidroxiprolina e hidroxilisina

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14
Q

Glucosilacion gracias a

A

Glucosa y galactosa

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15
Q

Hidroxilacion de prolil

A

Prolil hidroxilasa usando Fe2

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16
Q

Cadenas prepo-α

A

Facilita luz de RER dando pro-α

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17
Q

Pro-α1 y 2

A

Se trascriben en ARNm

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18
Q

ARNm se traduce a RER

A

En cadena prepo-α y en luz a pro-α

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19
Q

Pro-α hidroliza

A

Prolina o lisina

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20
Q

Hidroxilisina se glucosila con

A

Glucosa o galactosa

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21
Q

Se unen 3 pro-α

A

Formando enlaces disulfuro en C-terminal

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22
Q

Procolageno se secreta desde una vacula de golgi a

A

Matrix extracelular

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23
Q

La tropocolageno se da por

A

Procolageno con peptidasas

24
Q

Moleculas de tropocolageno forman

A

Colageno

25
Q

Para hidroxilacion de lisina y prolina se necesita

A

O2, Fe2 y vitC

26
Q

Sin vitC

A

Prolil hidroxilasa y lisil hidroxilasa no funcionan

27
Q

Equimosis por

A

Escorbuto

28
Q

Triple helice con C y N terminal forman

A

Propeptidos

29
Q

Lisil oxidasa contiene

A

Cu2

30
Q

Lisil oxidasa oxida a

A

Allisina e hidroxiallisina

31
Q

Alteracion en Cu

A

Sindrome de menkes o enfermedas de wilson

32
Q

Rompimiento de fibras de colageno

A

Colegenasas

33
Q

Defectos en sintesis de colagenos

A

Colagenopatias

34
Q

Sindrome de ehlers-danlos(sed)

A

Defctos hereditarios de colageno fibrilar(I, III,V)

35
Q

Extensibilidad de piel y hipermovilidad articular

A

SED V

36
Q

Forma vascular de SED

A

SED III

37
Q

Forma clasica y muscular son

A

Enfermedades autosomicas dominantes

38
Q

Enfermedad de huesos fragiles

A

Osteogenesis inperfecta

39
Q

80% de OI

A

Mutaciones en cadenas α1 y 2 del colagno I

40
Q

Remplazo mas recuente

A

Glicina por aminoacido voluminoso

41
Q

OI I

A

Esclerotica azul y fragilidad osea leve

42
Q

OI II

A

Letal, complicaciones en utero

43
Q

OI III

A

Fracturas al nacer y cifosis

44
Q

Polimero proteico insoluble

A

Elastina

45
Q

Elastina viene

A

Tropoelastina( 700 aa(glicina,alanina y valina))

46
Q

Elastina

A

No tiene tanta hidroxiprolina e hidroxilisina

47
Q

Tropoelastina interactua en MEC con

A

Fibrilina

48
Q

3 allisil + 1 lisilo forman

A

Desmosina

49
Q

Alteraciones en fibrilina-1

A

Sindrome de marfan

50
Q

Inhibe las peptidasas, proteasas o proteinasas

A

α1-antitrpsina (AAT)

51
Q

AAT importante en

A

Inhibir elastasa de neutrofilos

52
Q

Que hace la elastasa

A

Se libera en EEC y degrada paredes alveolares

53
Q

De domde salen las AAT

A

Higado

54
Q

Mutacion base purica GAG por AAG

A

Sustituye lisina por acido glutamico

55
Q

Mutacion que hace que AAT se pliege anormalmente y agrege en RER del higado

A

Variante Z

56
Q

Causa oxidacion e inactivacion de metionina

A

Tabaquisimo

BIOCA Team (25 decks)

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